GenomeRNAi

Phenotype information for gene 5261 (PHKG2)

Screen Title	Gene ID	Gene Symbol	Reagent ID	Score	Phenotype	Follow Up
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000000398	0,53	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Combinatorial effect with gemcitabine		PHKG2	PHKG2_A	-0,26	none	no
Reference Synthetic lethal RNAi screening identifies sensitizing targets for gemcitabine therapy in pancreatic cancer. Azorsa et al., 2009 Pancreatic cancer retains a poor prognosis among the gastrointestinal cancers. It affects 230,000 individuals worldwide, has a very high mortality rate, and remains one of the most challenging malignancies to treat successfully. Treatment with gemcitabine, the most widely used chemotherapeutic against pancreatic cancer, is not curative and resistance may occur. Combinations of gemcitabine with other chemotherapeutic drugs or biological agents have resulted in limited improvement. View Phenotypes Download PubMed Screen Details Stable ID: GR00225-A Screen Title: Combinatorial effect with gemcitabine Assay: Viability (synthetic lethal) Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MIA PaCa-2 Library: Qiagen, Validated kinase siRNA library version 1.0 Reagent Type: siRNA Score Type: log2 ratio Cutoff: 1.65 SD below mean ratio level Notes:
Melanogenesis	NM_000294	PHKG2	np	0,85	none	no
Reference Genome-wide siRNA-based functional genomics of pigmentation identifies novel genes and pathways that impact melanogenesis in human cells. Ganesan et al., 2008 Melanin protects the skin and eyes from the harmful effects of UV irradiation, protects neural cells from toxic insults, and is required for sound conduction in the inner ear. Aberrant regulation of melanogenesis underlies skin disorders (melasma and vitiligo), neurologic disorders (Parkinson''s disease), auditory disorders (Waardenburg''s syndrome), and opthalmologic disorders (age related macular degeneration). Much of the core synthetic machinery driving melanin production has been identified; however, the spectrum of gene products participating in melanogenesis in different physiological niches is poorly understood. Functional genomics based on RNA-mediated interference (RNAi) provides the opportunity to derive unbiased comprehensive collections of pharmaceutically tractable single gene targets supporting melanin production. In this study, we have combined a high-throughput, cell-based, one-well/one-gene screening platform with a genome-wide arrayed synthetic library of chemically synthesized, small interfering RNAs to identify novel biological pathways that govern melanin biogenesis in human melanocytes. Ninety-two novel genes that support pigment production were identified with a low false discovery rate. Secondary validation and preliminary mechanistic studies identified a large panel of targets that converge on tyrosinase expression and stability. Small molecule inhibition of a family of gene products in this class was sufficient to impair chronic tyrosinase expression in pigmented melanoma cells and UV-induced tyrosinase expression in primary melanocytes. Isolation of molecular machinery known to support autophagosome biosynthesis from this screen, together with in vitro and in vivo validation, exposed a close functional relationship between melanogenesis and autophagy. In summary, these studies illustrate the power of RNAi-based functional genomics to identify novel genes, pathways, and pharmacologic agents that impact a biological phenotype and operate outside of preconceived mechanistic relationships. View Phenotypes Download PubMed Screen Details Stable ID: GR00056-A Screen Title: Melanogenesis Assay: Melanin protein expression and viability Method: Absorbance and luminescence Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MNT-1 Library: Dharmacon, rp Reagent Type: siRNA Score Type: Normalized absorbance ratio Cutoff: > 2 standard deviations below mean Notes: Additional information about a secondary screen (retest to determine false-positive rate)
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000000399	0,13	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Hepatitis C virus replication (1)	5261	PHKG2	PL-50002	0,92	none	no
Reference A functional genomic screen identifies cellular cofactors of hepatitis C virus replication. Tai et al., 2009 Hepatitis C virus (HCV) chronically infects 3% of the world''s population, and complications from HCV are the leading indication for liver transplantation. Given the need for better anti-HCV therapies, one strategy is to identify and target cellular cofactors of the virus lifecycle. Using a genome-wide siRNA library, we identified 96 human genes that support HCV replication, with a significant number of them being involved in vesicle organization and biogenesis. Phosphatidylinositol 4-kinase PI4KA and multiple subunits of the COPI vesicle coat complex were among the genes identified. Consistent with this, pharmacologic inhibitors of COPI and PI4KA blocked HCV replication. Targeting hepcidin, a peptide critical for iron homeostasis, also affected HCV replication, which may explain the known dysregulation of iron homeostasis in HCV infection. The host cofactors for HCV replication identified in this study should serve as a useful resource in delineating new targets for anti-HCV therapies. View Phenotypes Download PubMed Screen Details Stable ID: GR00180-A-1 Screen Title: Hepatitis C virus replication (1) Assay: HCV replicon RNA copy number Method: Luminescence Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: Huh7/Rep-Feo Library: Dharmacon, siARRAY Human Genome siRNA Library Reagent Type: siRNA Score Type: q-value Cutoff: Complex criteria Notes:
Therapeutic kinase targets in neuroblastoma (4)	5261	PHKG2	PHKG2	0,45	Decreased substrate adherent cell growth	yes
Reference RNAi screen of the protein kinome identifies checkpoint kinase 1 (CHK1) as a therapeutic target in neuroblastoma. Cole et al., 2011 Neuroblastoma is a childhood cancer that is often fatal despite intense multimodality therapy. In an effort to identify therapeutic targets for this disease, we performed a comprehensive loss-of-function screen of the protein kinome. Thirty kinases showed significant cellular cytotoxicity when depleted, with loss of the cell cycle checkpoint kinase 1 (CHK1/CHEK1) being the most potent. CHK1 mRNA expression was higher in MYC-Neuroblastoma-related (MYCN)-amplified (P < 0.0001) and high-risk (P = 0.03) tumors. Western blotting revealed that CHK1 was constitutively phosphorylated at the ataxia telangiectasia response kinase target site Ser345 and the autophosphorylation site Ser296 in neuroblastoma cell lines. This pattern was also seen in six of eight high-risk primary tumors but not in control nonneuroblastoma cell lines or in seven of eight low-risk primary tumors. Neuroblastoma cells were sensitive to the two CHK1 inhibitors SB21807 and TCS2312, with median IC(50) values of 564 nM and 548 nM, respectively. In contrast, the control lines had high micromolar IC(50) values, indicating a strong correlation between CHK1 phosphorylation and CHK1 inhibitor sensitivity (P = 0.0004). Furthermore, cell cycle analysis revealed that CHK1 inhibition in neuroblastoma cells caused apoptosis during S-phase, consistent with its role in replication fork progression. CHK1 inhibitor sensitivity correlated with total MYC(N) protein levels, and inducing MYCN in retinal pigmented epithelial cells resulted in CHK1 phosphorylation, which caused growth inhibition when inhibited. These data show the power of a functional RNAi screen to identify tractable therapeutical targets in neuroblastoma and support CHK1 inhibition strategies in this disease. View Phenotypes Download PubMed Screen Details Stable ID: GR00193-A-4 Screen Title: Therapeutic kinase targets in neuroblastoma (4) Assay: Substrate adherent cell growth Method: rp Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: NLF Library: Thermo Scientific, Kinase siGenome library Reagent Type: siRNA Score Type: Relative growth Cutoff: 0.5 standard deviations below mean Notes:
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000000400	1,43	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000010056	-2,67	Decreased viability	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (1)		PHKG2	TRCN0000000398	-0,01	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-1 Screen Title: Proliferation of cells with active beta-catenin (1) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF7 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Ciliogenesis and cilium length (1)	5261	PHKG2	110737	np	none	no
Reference Functional genomic screen for modulators of ciliogenesis and cilium length. Kim et al., 2010 Primary cilia are evolutionarily conserved cellular organelles that organize diverse signalling pathways. Defects in the formation or function of primary cilia are associated with a spectrum of human diseases and developmental abnormalities. Genetic screens in model organisms have discovered core machineries of cilium assembly and maintenance. However, regulatory molecules that coordinate the biogenesis of primary cilia with other cellular processes, including cytoskeletal organization, vesicle trafficking and cell-cell adhesion, remain to be identified. Here we report the results of a functional genomic screen using RNA interference (RNAi) to identify human genes involved in ciliogenesis control. The screen identified 36 positive and 13 negative ciliogenesis modulators, which include molecules involved in actin dynamics and vesicle trafficking. Further investigation demonstrated that blocking actin assembly facilitates ciliogenesis by stabilizing the pericentrosomal preciliary compartment (PPC), a previously uncharacterized compact vesiculotubular structure storing transmembrane proteins destined for cilia during the early phase of ciliogenesis. The PPC was labelled by recycling endosome markers. Moreover, knockdown of modulators that are involved in the endocytic recycling pathway affected the formation of the PPC as well as ciliogenesis. Our results uncover a critical regulatory step that couples actin dynamics and endocytic recycling with ciliogenesis, and also provides potential target molecules for future study. View Phenotypes Download PubMed Screen Details Stable ID: GR00149-A-1 Screen Title: Ciliogenesis and cilium length (1) Assay: Smoothed protein expression Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: htRPE Library: Ambion, Human druggable genome siRNA library V3.1 Reagent Type: siRNA Score Type: Normalized percent inhibition Cutoff: > 1.5 OR < -1.5 standard deviations from mean Notes:
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000010068	-0,33	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Ciliogenesis and cilium length (1)	5261	PHKG2	118254	69,36	none	no
Reference Functional genomic screen for modulators of ciliogenesis and cilium length. Kim et al., 2010 Primary cilia are evolutionarily conserved cellular organelles that organize diverse signalling pathways. Defects in the formation or function of primary cilia are associated with a spectrum of human diseases and developmental abnormalities. Genetic screens in model organisms have discovered core machineries of cilium assembly and maintenance. However, regulatory molecules that coordinate the biogenesis of primary cilia with other cellular processes, including cytoskeletal organization, vesicle trafficking and cell-cell adhesion, remain to be identified. Here we report the results of a functional genomic screen using RNA interference (RNAi) to identify human genes involved in ciliogenesis control. The screen identified 36 positive and 13 negative ciliogenesis modulators, which include molecules involved in actin dynamics and vesicle trafficking. Further investigation demonstrated that blocking actin assembly facilitates ciliogenesis by stabilizing the pericentrosomal preciliary compartment (PPC), a previously uncharacterized compact vesiculotubular structure storing transmembrane proteins destined for cilia during the early phase of ciliogenesis. The PPC was labelled by recycling endosome markers. Moreover, knockdown of modulators that are involved in the endocytic recycling pathway affected the formation of the PPC as well as ciliogenesis. Our results uncover a critical regulatory step that couples actin dynamics and endocytic recycling with ciliogenesis, and also provides potential target molecules for future study. View Phenotypes Download PubMed Screen Details Stable ID: GR00149-A-1 Screen Title: Ciliogenesis and cilium length (1) Assay: Smoothed protein expression Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: htRPE Library: Ambion, Human druggable genome siRNA library V3.1 Reagent Type: siRNA Score Type: Normalized percent inhibition Cutoff: > 1.5 OR < -1.5 standard deviations from mean Notes:
Ciliogenesis and cilium length (1)	5261	PHKG2	289133	-11,01	none	no
Reference Functional genomic screen for modulators of ciliogenesis and cilium length. Kim et al., 2010 Primary cilia are evolutionarily conserved cellular organelles that organize diverse signalling pathways. Defects in the formation or function of primary cilia are associated with a spectrum of human diseases and developmental abnormalities. Genetic screens in model organisms have discovered core machineries of cilium assembly and maintenance. However, regulatory molecules that coordinate the biogenesis of primary cilia with other cellular processes, including cytoskeletal organization, vesicle trafficking and cell-cell adhesion, remain to be identified. Here we report the results of a functional genomic screen using RNA interference (RNAi) to identify human genes involved in ciliogenesis control. The screen identified 36 positive and 13 negative ciliogenesis modulators, which include molecules involved in actin dynamics and vesicle trafficking. Further investigation demonstrated that blocking actin assembly facilitates ciliogenesis by stabilizing the pericentrosomal preciliary compartment (PPC), a previously uncharacterized compact vesiculotubular structure storing transmembrane proteins destined for cilia during the early phase of ciliogenesis. The PPC was labelled by recycling endosome markers. Moreover, knockdown of modulators that are involved in the endocytic recycling pathway affected the formation of the PPC as well as ciliogenesis. Our results uncover a critical regulatory step that couples actin dynamics and endocytic recycling with ciliogenesis, and also provides potential target molecules for future study. View Phenotypes Download PubMed Screen Details Stable ID: GR00149-A-1 Screen Title: Ciliogenesis and cilium length (1) Assay: Smoothed protein expression Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: htRPE Library: Ambion, Human druggable genome siRNA library V3.1 Reagent Type: siRNA Score Type: Normalized percent inhibition Cutoff: > 1.5 OR < -1.5 standard deviations from mean Notes:
Self-renewal and pluripotency in human embryonic stem cells (1)	NM_000294	PHKG2	M-004881-00	-0,68	none	no
Reference A genome-wide RNAi screen reveals determinants of human embryonic stem cell identity. Chia et al., 2010 The derivation of human ES cells (hESCs) from human blastocysts represents one of the milestones in stem cell biology. The full potential of hESCs in research and clinical applications requires a detailed understanding of the genetic network that governs the unique properties of hESCs. Here, we report a genome-wide RNA interference screen to identify genes which regulate self-renewal and pluripotency properties in hESCs. Interestingly, functionally distinct complexes involved in transcriptional regulation and chromatin remodelling are among the factors identified in the screen. To understand the roles of these potential regulators of hESCs, we studied transcription factor PRDM14 to gain new insights into its functional roles in the regulation of pluripotency. We showed that PRDM14 regulates directly the expression of key pluripotency gene POU5F1 through its proximal enhancer. Genome-wide location profiling experiments revealed that PRDM14 colocalized extensively with other key transcription factors such as OCT4, NANOG and SOX2, indicating that PRDM14 is integrated into the core transcriptional regulatory network. More importantly, in a gain-of-function assay, we showed that PRDM14 is able to enhance the efficiency of reprogramming of human fibroblasts in conjunction with OCT4, SOX2 and KLF4. Altogether, our study uncovers a wealth of novel hESC regulators wherein PRDM14 exemplifies a key transcription factor required for the maintenance of hESC identity and the reacquisition of pluripotency in human somatic cells. View Phenotypes Download PubMed Screen Details Stable ID: GR00184-A-1 Screen Title: Self-renewal and pluripotency in human embryonic stem cells (1) Assay: POU5F1 protein expression Method: Fluorescence Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: hESC H1 Library: Dharmacon, SMARTpool siRNA library Reagent Type: siRNA Score Type: Z-score Cutoff: < -2 Notes:
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000055433	0,17	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000010065	0,2	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (1)		PHKG2	TRCN0000010068	0,51	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-1 Screen Title: Proliferation of cells with active beta-catenin (1) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF7 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Therapeutic kinase targets in neuroblastoma (1)	5261	PHKG2	PHKG2	0,4	Decreased substrate adherent cell growth	yes
Reference RNAi screen of the protein kinome identifies checkpoint kinase 1 (CHK1) as a therapeutic target in neuroblastoma. Cole et al., 2011 Neuroblastoma is a childhood cancer that is often fatal despite intense multimodality therapy. In an effort to identify therapeutic targets for this disease, we performed a comprehensive loss-of-function screen of the protein kinome. Thirty kinases showed significant cellular cytotoxicity when depleted, with loss of the cell cycle checkpoint kinase 1 (CHK1/CHEK1) being the most potent. CHK1 mRNA expression was higher in MYC-Neuroblastoma-related (MYCN)-amplified (P < 0.0001) and high-risk (P = 0.03) tumors. Western blotting revealed that CHK1 was constitutively phosphorylated at the ataxia telangiectasia response kinase target site Ser345 and the autophosphorylation site Ser296 in neuroblastoma cell lines. This pattern was also seen in six of eight high-risk primary tumors but not in control nonneuroblastoma cell lines or in seven of eight low-risk primary tumors. Neuroblastoma cells were sensitive to the two CHK1 inhibitors SB21807 and TCS2312, with median IC(50) values of 564 nM and 548 nM, respectively. In contrast, the control lines had high micromolar IC(50) values, indicating a strong correlation between CHK1 phosphorylation and CHK1 inhibitor sensitivity (P = 0.0004). Furthermore, cell cycle analysis revealed that CHK1 inhibition in neuroblastoma cells caused apoptosis during S-phase, consistent with its role in replication fork progression. CHK1 inhibitor sensitivity correlated with total MYC(N) protein levels, and inducing MYCN in retinal pigmented epithelial cells resulted in CHK1 phosphorylation, which caused growth inhibition when inhibited. These data show the power of a functional RNAi screen to identify tractable therapeutical targets in neuroblastoma and support CHK1 inhibition strategies in this disease. View Phenotypes Download PubMed Screen Details Stable ID: GR00193-A-1 Screen Title: Therapeutic kinase targets in neuroblastoma (1) Assay: Substrate adherent cell growth Method: rp Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: EBC1 Library: Thermo Scientific, Kinase siGenome library Reagent Type: siRNA Score Type: Relative growth Cutoff: 0.5 standard deviations below mean Notes:
Salmonella enterica subspecies 1 serovar Typhimurium invasion (1)	5261	PHKG2	np	-0,21	none	no
Reference RNAi screen of Salmonella invasion shows role of COPI in membrane targeting of cholesterol and Cdc42. Misselwitz et al., 2011 The pathogen Salmonella Typhimurium is a common cause of diarrhea and invades the gut tissue by injecting a cocktail of virulence factors into epithelial cells, triggering actin rearrangements, membrane ruffling and pathogen entry. One of these factors is SopE, a G-nucleotide exchange factor for the host cellular Rho GTPases Rac1 and Cdc42. How SopE mediates cellular invasion is incompletely understood. Using genome-scale RNAi screening we identified 72 known and novel host cell proteins affecting SopE-mediated entry. Follow-up assays assigned these ''hits'' to particular steps of the invasion process; i.e., binding, effector injection, membrane ruffling, membrane closure and maturation of the Salmonella-containing vacuole. Depletion of the COPI complex revealed a unique effect on virulence factor injection and membrane ruffling. Both effects are attributable to mislocalization of cholesterol, sphingolipids, Rac1 and Cdc42 away from the plasma membrane into a large intracellular compartment. Equivalent results were obtained with the vesicular stomatitis virus. Therefore, COPI-facilitated maintenance of lipids may represent a novel, unifying mechanism essential for a wide range of pathogens, offering opportunities for designing new drugs. View Phenotypes Download PubMed Screen Details Stable ID: GR00133-A-1 Screen Title: Salmonella enterica subspecies 1 serovar Typhimurium invasion (1) Assay: Gentamycin protection invasion assay Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: HeLa Library: Qiagen, Druggable genome library V2.0 Reagent Type: siRNA Score Type: log2 median Cutoff: Complex criteria Notes:
Proliferation of cells with active beta-catenin (1)		PHKG2	TRCN0000010056	-2,49	Decreased viability	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-1 Screen Title: Proliferation of cells with active beta-catenin (1) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF7 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Ciliogenesis and cilium length (1)	5261	PHKG2	118293	81,47	none	no
Reference Functional genomic screen for modulators of ciliogenesis and cilium length. Kim et al., 2010 Primary cilia are evolutionarily conserved cellular organelles that organize diverse signalling pathways. Defects in the formation or function of primary cilia are associated with a spectrum of human diseases and developmental abnormalities. Genetic screens in model organisms have discovered core machineries of cilium assembly and maintenance. However, regulatory molecules that coordinate the biogenesis of primary cilia with other cellular processes, including cytoskeletal organization, vesicle trafficking and cell-cell adhesion, remain to be identified. Here we report the results of a functional genomic screen using RNA interference (RNAi) to identify human genes involved in ciliogenesis control. The screen identified 36 positive and 13 negative ciliogenesis modulators, which include molecules involved in actin dynamics and vesicle trafficking. Further investigation demonstrated that blocking actin assembly facilitates ciliogenesis by stabilizing the pericentrosomal preciliary compartment (PPC), a previously uncharacterized compact vesiculotubular structure storing transmembrane proteins destined for cilia during the early phase of ciliogenesis. The PPC was labelled by recycling endosome markers. Moreover, knockdown of modulators that are involved in the endocytic recycling pathway affected the formation of the PPC as well as ciliogenesis. Our results uncover a critical regulatory step that couples actin dynamics and endocytic recycling with ciliogenesis, and also provides potential target molecules for future study. View Phenotypes Download PubMed Screen Details Stable ID: GR00149-A-1 Screen Title: Ciliogenesis and cilium length (1) Assay: Smoothed protein expression Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: htRPE Library: Ambion, Human druggable genome siRNA library V3.1 Reagent Type: siRNA Score Type: Normalized percent inhibition Cutoff: > 1.5 OR < -1.5 standard deviations from mean Notes:
Self-renewal and pluripotency in human embryonic stem cells (1)	XM_373675	LOC90835	M-030737-00	-0,1	none	no
Reference A genome-wide RNAi screen reveals determinants of human embryonic stem cell identity. Chia et al., 2010 The derivation of human ES cells (hESCs) from human blastocysts represents one of the milestones in stem cell biology. The full potential of hESCs in research and clinical applications requires a detailed understanding of the genetic network that governs the unique properties of hESCs. Here, we report a genome-wide RNA interference screen to identify genes which regulate self-renewal and pluripotency properties in hESCs. Interestingly, functionally distinct complexes involved in transcriptional regulation and chromatin remodelling are among the factors identified in the screen. To understand the roles of these potential regulators of hESCs, we studied transcription factor PRDM14 to gain new insights into its functional roles in the regulation of pluripotency. We showed that PRDM14 regulates directly the expression of key pluripotency gene POU5F1 through its proximal enhancer. Genome-wide location profiling experiments revealed that PRDM14 colocalized extensively with other key transcription factors such as OCT4, NANOG and SOX2, indicating that PRDM14 is integrated into the core transcriptional regulatory network. More importantly, in a gain-of-function assay, we showed that PRDM14 is able to enhance the efficiency of reprogramming of human fibroblasts in conjunction with OCT4, SOX2 and KLF4. Altogether, our study uncovers a wealth of novel hESC regulators wherein PRDM14 exemplifies a key transcription factor required for the maintenance of hESC identity and the reacquisition of pluripotency in human somatic cells. View Phenotypes Download PubMed Screen Details Stable ID: GR00184-A-1 Screen Title: Self-renewal and pluripotency in human embryonic stem cells (1) Assay: POU5F1 protein expression Method: Fluorescence Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: hESC H1 Library: Dharmacon, SMARTpool siRNA library Reagent Type: siRNA Score Type: Z-score Cutoff: < -2 Notes:
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000000398	0,43	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000055433	-0,21	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Combinatorial effect with gemcitabine		PHKG2	PHKG2_B	-0,32	none	no
Reference Synthetic lethal RNAi screening identifies sensitizing targets for gemcitabine therapy in pancreatic cancer. Azorsa et al., 2009 Pancreatic cancer retains a poor prognosis among the gastrointestinal cancers. It affects 230,000 individuals worldwide, has a very high mortality rate, and remains one of the most challenging malignancies to treat successfully. Treatment with gemcitabine, the most widely used chemotherapeutic against pancreatic cancer, is not curative and resistance may occur. Combinations of gemcitabine with other chemotherapeutic drugs or biological agents have resulted in limited improvement. View Phenotypes Download PubMed Screen Details Stable ID: GR00225-A Screen Title: Combinatorial effect with gemcitabine Assay: Viability (synthetic lethal) Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MIA PaCa-2 Library: Qiagen, Validated kinase siRNA library version 1.0 Reagent Type: siRNA Score Type: log2 ratio Cutoff: 1.65 SD below mean ratio level Notes:
Proliferation of cells with active beta-catenin (1)		PHKG2	TRCN0000000400	1,23	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-1 Screen Title: Proliferation of cells with active beta-catenin (1) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF7 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Combinatorial effect with paclitaxel	NM_000294	PHKG2	np	0,96	none	no
Reference Synthetic lethal screen identification of chemosensitizer loci in cancer cells. Whitehurst et al., 2007 Abundant evidence suggests that a unifying principle governing the molecular pathology of cancer is the co-dependent aberrant regulation of core machinery driving proliferation and suppressing apoptosis. Anomalous proteins engaged in support of this tumorigenic regulatory environment most probably represent optimal intervention targets in a heterogeneous population of cancer cells. The advent of RNA-mediated interference (RNAi)-based functional genomics provides the opportunity to derive unbiased comprehensive collections of validated gene targets supporting critical biological systems outside the framework of preconceived notions of mechanistic relationships. We have combined a high-throughput cell-based one-well/one-gene screening platform with a genome-wide synthetic library of chemically synthesized small interfering RNAs for systematic interrogation of the molecular underpinnings of cancer cell chemoresponsiveness. NCI-H1155, a human non-small-cell lung cancer line, was employed in a paclitaxel-dependent synthetic lethal screen designed to identify gene targets that specifically reduce cell viability in the presence of otherwise sublethal concentrations of paclitaxel. Using a stringent objective statistical algorithm to reduce false discovery rates below 5%, we isolated a panel of 87 genes that represent major focal points of the autonomous response of cancer cells to the abrogation of microtubule dynamics. Here we show that several of these targets sensitize lung cancer cells to paclitaxel concentrations 1,000-fold lower than otherwise required for a significant response, and we identify mechanistic relationships between cancer-associated aberrant gene expression programmes and the basic cellular machinery required for robust mitotic progression. View Phenotypes Download PubMed Screen Details Stable ID: GR00054-A Screen Title: Combinatorial effect with paclitaxel Assay: Viability (synthetic lethal) Method: ATP level Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: NCI-H1155 Library: Dharmacon, # G-005000-01 Reagent Type: siRNA Score Type: Paclitaxel/control ratio Cutoff: Complex criteria Notes: Additional information about 87 high-confidence hits
Proliferation of cells with active beta-catenin (1)		PHKG2	TRCN0000055433	-0,81	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-1 Screen Title: Proliferation of cells with active beta-catenin (1) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF7 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Focal adhesion formation	5261	PHKG2	np	sp	Decreased focal adhesion (FA) abundance, increased peripheral FA formation, increased cell spreading	no
Reference Multiparametric analysis of focal adhesion formation by RNAi-mediated gene knockdown. Winograd-Katz et al., 2009 Cell adhesion to the extracellular matrix is mediated by elaborate networks of multiprotein complexes consisting of adhesion receptors, cytoskeletal components, signaling molecules, and diverse adaptor proteins. To explore how specific molecular pathways function in the assembly of focal adhesions (FAs), we performed a high-throughput, high-resolution, microscopy-based screen. We used small interfering RNAs (siRNAs) to target human kinases, phosphatases, and migration- and adhesion-related genes. Multiparametric image analysis of control and of siRNA-treated cells revealed major correlations between distinct morphological FA features. Clustering analysis identified different gene families whose perturbation induced similar effects, some of which uncoupled the interfeature correlations. Based on these findings, we propose a model for the molecular hierarchy of FA formation, and tested its validity by dynamic analysis of FA formation and turnover. This study provides a comprehensive information resource on the molecular regulation of multiple cell adhesion features, and sheds light on signaling mechanisms regulating the formation of integrin adhesions. View Phenotypes Download PubMed Screen Details Stable ID: GR00210-A Screen Title: Focal adhesion formation Assay: paxillin protein expression Method: Fluorescence Scope: Kinases, phosphatases and selected genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: HeLa Library: Thermo Fisher Scientific, SMARTpool siARRAY siRNA Libraries Reagent Type: siRNA Score Type: Z-score Cutoff: > 3.5 OR < -3.5 Notes:
T cell chemotaxis	NM_000294	PHKG2	np	np	none	no
Reference Synaptotagmin-mediated vesicle fusion regulates cell migration. Colvin et al., 2010 Chemokines and other chemoattractants direct leukocyte migration and are essential for the development and delivery of immune and inflammatory responses. To probe the molecular mechanisms that underlie chemoattractant-guided migration, we did an RNA-mediated interference screen that identified several members of the synaptotagmin family of calcium-sensing vesicle-fusion proteins as mediators of cell migration: SYT7 and SYTL5 were positive regulators of chemotaxis, whereas SYT2 was a negative regulator of chemotaxis. SYT7-deficient leukocytes showed less migration in vitro and in a gout model in vivo. Chemoattractant-induced calcium-dependent lysosomal fusion was impaired in SYT7-deficient neutrophils. In a chemokine gradient, SYT7-deficient lymphocytes accumulated lysosomes in their uropods and had impaired uropod release. Our data identify a molecular pathway required for chemotaxis that links chemoattractant-induced calcium flux to exocytosis and uropod release. View Phenotypes Download PubMed Screen Details Stable ID: GR00141-A Screen Title: T cell chemotaxis Assay: Cell migration Method: Fluorescence Scope: Kinases, phosphatases and selected genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: SupT1 Library: TRC, shRNA Library Reagent Type: shRNA Score Type: Chemotactic index Cutoff: > 1 standard deviation from plate mean by at least 2 shRNAs Notes:
Proliferation of cells with active beta-catenin (1)		PHKG2	TRCN0000010065	1,33	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-1 Screen Title: Proliferation of cells with active beta-catenin (1) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF7 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
tau phosphorylation		PHKG2	PHKG2 s2	sp	none	no
Reference High-content siRNA screening of the kinome identifies kinases involved in Alzheimer's disease-related tau hyperphosphorylation. Azorsa et al., 2010 Neurofibrillary tangles (NFT), a cardinal neuropathological feature of Alzheimer''s disease (AD) that is highly correlated with synaptic loss and dementia severity, appear to be partly attributable to increased phosphorylation of the microtubule stabilizing protein tau at certain AD-related residues. Identifying the kinases involved in the pathologic phosphorylation of tau may provide targets at which to aim new AD-modifying treatments. View Phenotypes Download PubMed Screen Details Stable ID: GR00143-A Screen Title: tau phosphorylation Assay: Total tau and 12E8 tau protein expression Method: Fluorescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: H4 overexpressing 4RON tau Library: Qiagen, Validated human kinase siRNA Set 2.0 Reagent Type: siRNA Score Type: p-value Cutoff: Complex criteria Notes:
Combinatorial effect with gemcitabine		PHKG2	PHKG2_A	-1,06	none	no
Reference Synthetic lethal RNAi screening identifies sensitizing targets for gemcitabine therapy in pancreatic cancer. Azorsa et al., 2009 Pancreatic cancer retains a poor prognosis among the gastrointestinal cancers. It affects 230,000 individuals worldwide, has a very high mortality rate, and remains one of the most challenging malignancies to treat successfully. Treatment with gemcitabine, the most widely used chemotherapeutic against pancreatic cancer, is not curative and resistance may occur. Combinations of gemcitabine with other chemotherapeutic drugs or biological agents have resulted in limited improvement. View Phenotypes Download PubMed Screen Details Stable ID: GR00225-A Screen Title: Combinatorial effect with gemcitabine Assay: Viability (synthetic lethal) Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MIA PaCa-2 Library: Qiagen, Validated kinase siRNA library version 1.0 Reagent Type: siRNA Score Type: log2 ratio Cutoff: 1.65 SD below mean ratio level Notes:
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000000400	-0,11	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Ciliogenesis and cilium length (1)	5261	PHKG2	110737	55,35	none	no
Reference Functional genomic screen for modulators of ciliogenesis and cilium length. Kim et al., 2010 Primary cilia are evolutionarily conserved cellular organelles that organize diverse signalling pathways. Defects in the formation or function of primary cilia are associated with a spectrum of human diseases and developmental abnormalities. Genetic screens in model organisms have discovered core machineries of cilium assembly and maintenance. However, regulatory molecules that coordinate the biogenesis of primary cilia with other cellular processes, including cytoskeletal organization, vesicle trafficking and cell-cell adhesion, remain to be identified. Here we report the results of a functional genomic screen using RNA interference (RNAi) to identify human genes involved in ciliogenesis control. The screen identified 36 positive and 13 negative ciliogenesis modulators, which include molecules involved in actin dynamics and vesicle trafficking. Further investigation demonstrated that blocking actin assembly facilitates ciliogenesis by stabilizing the pericentrosomal preciliary compartment (PPC), a previously uncharacterized compact vesiculotubular structure storing transmembrane proteins destined for cilia during the early phase of ciliogenesis. The PPC was labelled by recycling endosome markers. Moreover, knockdown of modulators that are involved in the endocytic recycling pathway affected the formation of the PPC as well as ciliogenesis. Our results uncover a critical regulatory step that couples actin dynamics and endocytic recycling with ciliogenesis, and also provides potential target molecules for future study. View Phenotypes Download PubMed Screen Details Stable ID: GR00149-A-1 Screen Title: Ciliogenesis and cilium length (1) Assay: Smoothed protein expression Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: htRPE Library: Ambion, Human druggable genome siRNA library V3.1 Reagent Type: siRNA Score Type: Normalized percent inhibition Cutoff: > 1.5 OR < -1.5 standard deviations from mean Notes:
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000000399	-0,19	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Cell division (1)	ENSG00000156873	PHKG2	ENSG00000156873	sp	none	no
Reference Genome-scale RNAi profiling of cell division in human tissue culture cells. Kittler et al., 2007 Cell division is fundamental for all organisms. Here we report a genome-scale RNA-mediated interference screen in HeLa cells designed to identify human genes that are important for cell division. We have used a library of endoribonuclease-prepared short interfering RNAs for gene silencing and have used DNA content analysis to identify genes that induced cell cycle arrest or altered ploidy on silencing. Validation and secondary assays were performed to generate a nine-parameter loss-of-function phenoprint for each of the genes. These phenotypic signatures allowed the assignment of genes to specific functional classes by combining hierarchical clustering, cross-species analysis and proteomic data mining. We highlight the richness of our dataset by ascribing novel functions to genes in mitosis and cytokinesis. In particular, we identify two evolutionarily conserved transcriptional regulatory networks that govern cytokinesis. Our work provides an experimental framework from which the systematic analysis of novel genes necessary for cell division in human cells can begin. View Phenotypes Download PubMed Screen Details Stable ID: GR00098-A-1 Screen Title: Cell division (1) Assay: Cell number and DNA content Method: Laser scanning cytometry Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: HeLa Library: Custom-made, rp Reagent Type: esiRNA Score Type: Complex, sp Cutoff: Complex criteria Notes:
Therapeutic kinase targets in neuroblastoma (3)	5261	PHKG2	PHKG2	0,82	Decreased substrate adherent cell growth	yes
Reference RNAi screen of the protein kinome identifies checkpoint kinase 1 (CHK1) as a therapeutic target in neuroblastoma. Cole et al., 2011 Neuroblastoma is a childhood cancer that is often fatal despite intense multimodality therapy. In an effort to identify therapeutic targets for this disease, we performed a comprehensive loss-of-function screen of the protein kinome. Thirty kinases showed significant cellular cytotoxicity when depleted, with loss of the cell cycle checkpoint kinase 1 (CHK1/CHEK1) being the most potent. CHK1 mRNA expression was higher in MYC-Neuroblastoma-related (MYCN)-amplified (P < 0.0001) and high-risk (P = 0.03) tumors. Western blotting revealed that CHK1 was constitutively phosphorylated at the ataxia telangiectasia response kinase target site Ser345 and the autophosphorylation site Ser296 in neuroblastoma cell lines. This pattern was also seen in six of eight high-risk primary tumors but not in control nonneuroblastoma cell lines or in seven of eight low-risk primary tumors. Neuroblastoma cells were sensitive to the two CHK1 inhibitors SB21807 and TCS2312, with median IC(50) values of 564 nM and 548 nM, respectively. In contrast, the control lines had high micromolar IC(50) values, indicating a strong correlation between CHK1 phosphorylation and CHK1 inhibitor sensitivity (P = 0.0004). Furthermore, cell cycle analysis revealed that CHK1 inhibition in neuroblastoma cells caused apoptosis during S-phase, consistent with its role in replication fork progression. CHK1 inhibitor sensitivity correlated with total MYC(N) protein levels, and inducing MYCN in retinal pigmented epithelial cells resulted in CHK1 phosphorylation, which caused growth inhibition when inhibited. These data show the power of a functional RNAi screen to identify tractable therapeutical targets in neuroblastoma and support CHK1 inhibition strategies in this disease. View Phenotypes Download PubMed Screen Details Stable ID: GR00193-A-3 Screen Title: Therapeutic kinase targets in neuroblastoma (3) Assay: Substrate adherent cell growth Method: rp Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: SKNAS Library: Thermo Scientific, Kinase siGenome library Reagent Type: siRNA Score Type: Relative growth Cutoff: 0.5 standard deviations below mean Notes:
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000010065	-0,06	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (1)		PHKG2	TRCN0000000399	-0,51	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-1 Screen Title: Proliferation of cells with active beta-catenin (1) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF7 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Human papillomavirus oncogene expression regulation (1)	90835	LOC90835	M-030737-00	-0,62	none	no
Reference Genome-wide siRNA screen identifies SMCX, EP400, and Brd4 as E2-dependent regulators of human papillomavirus oncogene expression. Smith et al., 2010 An essential step in the pathogenesis of human papillomavirus (HPV)-associated cancers is the dysregulated expression of the viral oncogenes. The papillomavirus E2 protein can silence the long control region (LCR) promoter that controls viral E6 and E7 oncogene expression. The mechanisms by which E2 represses oncogene expression and the cellular factors through which E2 mediates this silencing are largely unknown. We conducted an unbiased, genome-wide siRNA screen and series of secondary screens that identified 96 cellular genes that contribute to the repression of the HPV LCR. In addition to confirming a role for the E2-binding bromodomain protein Brd4 in E2-mediated silencing, we identified a number of genes that have not previously been implicated in E2 repression, including the demethylase JARID1C/SMCX as well as EP400, a component of the NuA4/TIP60 histone acetyltransferase complex. Each of these genes contributes independently and additively to E2-mediated silencing, indicating that E2 functions through several distinct cellular complexes to repress E6 and E7 expression. View Phenotypes Download PubMed Screen Details Stable ID: GR00197-A-1 Screen Title: Human papillomavirus oncogene expression regulation (1) Assay: HPV18 LCR reporter activity Method: Luminescence Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: C33A/BE2/18LCR c4 Library: Dharmacon, Human siGENOME SMARTpool library Reagent Type: siRNA Score Type: Z-score Cutoff: >= 2 Notes: Author-submitted data; Phenotype strength according to Z-scores: weak: 2 - 3; moderate: 3 - 5; strong: > 5
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000010056	0,88	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000000401	0,32	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Ciliogenesis and cilium length (1)	5261	PHKG2	118293	64,91	none	no
Reference Functional genomic screen for modulators of ciliogenesis and cilium length. Kim et al., 2010 Primary cilia are evolutionarily conserved cellular organelles that organize diverse signalling pathways. Defects in the formation or function of primary cilia are associated with a spectrum of human diseases and developmental abnormalities. Genetic screens in model organisms have discovered core machineries of cilium assembly and maintenance. However, regulatory molecules that coordinate the biogenesis of primary cilia with other cellular processes, including cytoskeletal organization, vesicle trafficking and cell-cell adhesion, remain to be identified. Here we report the results of a functional genomic screen using RNA interference (RNAi) to identify human genes involved in ciliogenesis control. The screen identified 36 positive and 13 negative ciliogenesis modulators, which include molecules involved in actin dynamics and vesicle trafficking. Further investigation demonstrated that blocking actin assembly facilitates ciliogenesis by stabilizing the pericentrosomal preciliary compartment (PPC), a previously uncharacterized compact vesiculotubular structure storing transmembrane proteins destined for cilia during the early phase of ciliogenesis. The PPC was labelled by recycling endosome markers. Moreover, knockdown of modulators that are involved in the endocytic recycling pathway affected the formation of the PPC as well as ciliogenesis. Our results uncover a critical regulatory step that couples actin dynamics and endocytic recycling with ciliogenesis, and also provides potential target molecules for future study. View Phenotypes Download PubMed Screen Details Stable ID: GR00149-A-1 Screen Title: Ciliogenesis and cilium length (1) Assay: Smoothed protein expression Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: htRPE Library: Ambion, Human druggable genome siRNA library V3.1 Reagent Type: siRNA Score Type: Normalized percent inhibition Cutoff: > 1.5 OR < -1.5 standard deviations from mean Notes:
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000000400	0,53	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Aryl hydrocarbon receptor (AhR) transduction pathway regulation	5261	PHKG2	PHKG2_2 PHKG2_1 PHKG2_3	np	none	no
Reference RNAi-based screening identifies kinases interfering with dioxin-mediated up-regulation of CYP1A1 activity. Gilot et al., 2011 The aryl hydrocarbon receptor (AhR) is a transcription factor activated by several environmental pollutants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and involved in carcinogenesis and various physiological processes, including immune response and endocrine functions. Characterization of kinases-related AhR transduction pathway remains an important purpose. View Phenotypes Download PubMed Screen Details Stable ID: GR00155-A Screen Title: Aryl hydrocarbon receptor (AhR) transduction pathway regulation Assay: TCDD-induced CYP1A1-related EROD activity and cell viability Method: Fluorescence and methylene blue Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF-7 Library: Sigma-Genesys, MISSION siRNA Human Kinase Panel library Reagent Type: siRNA Score Type: Z-score Cutoff: Top 150 for >= 2 of 3 siRNAs AND no effect on cell proliferation Notes:
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000010069	0,42	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Ciliogenesis and cilium length (1)	5261	PHKG2	118254	55,02	none	no
Reference Functional genomic screen for modulators of ciliogenesis and cilium length. Kim et al., 2010 Primary cilia are evolutionarily conserved cellular organelles that organize diverse signalling pathways. Defects in the formation or function of primary cilia are associated with a spectrum of human diseases and developmental abnormalities. Genetic screens in model organisms have discovered core machineries of cilium assembly and maintenance. However, regulatory molecules that coordinate the biogenesis of primary cilia with other cellular processes, including cytoskeletal organization, vesicle trafficking and cell-cell adhesion, remain to be identified. Here we report the results of a functional genomic screen using RNA interference (RNAi) to identify human genes involved in ciliogenesis control. The screen identified 36 positive and 13 negative ciliogenesis modulators, which include molecules involved in actin dynamics and vesicle trafficking. Further investigation demonstrated that blocking actin assembly facilitates ciliogenesis by stabilizing the pericentrosomal preciliary compartment (PPC), a previously uncharacterized compact vesiculotubular structure storing transmembrane proteins destined for cilia during the early phase of ciliogenesis. The PPC was labelled by recycling endosome markers. Moreover, knockdown of modulators that are involved in the endocytic recycling pathway affected the formation of the PPC as well as ciliogenesis. Our results uncover a critical regulatory step that couples actin dynamics and endocytic recycling with ciliogenesis, and also provides potential target molecules for future study. View Phenotypes Download PubMed Screen Details Stable ID: GR00149-A-1 Screen Title: Ciliogenesis and cilium length (1) Assay: Smoothed protein expression Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: htRPE Library: Ambion, Human druggable genome siRNA library V3.1 Reagent Type: siRNA Score Type: Normalized percent inhibition Cutoff: > 1.5 OR < -1.5 standard deviations from mean Notes:
Human papillomavirus oncogene expression regulation (1)	5261	PHKG2	M-004881-00	1,11	none	no
Reference Genome-wide siRNA screen identifies SMCX, EP400, and Brd4 as E2-dependent regulators of human papillomavirus oncogene expression. Smith et al., 2010 An essential step in the pathogenesis of human papillomavirus (HPV)-associated cancers is the dysregulated expression of the viral oncogenes. The papillomavirus E2 protein can silence the long control region (LCR) promoter that controls viral E6 and E7 oncogene expression. The mechanisms by which E2 represses oncogene expression and the cellular factors through which E2 mediates this silencing are largely unknown. We conducted an unbiased, genome-wide siRNA screen and series of secondary screens that identified 96 cellular genes that contribute to the repression of the HPV LCR. In addition to confirming a role for the E2-binding bromodomain protein Brd4 in E2-mediated silencing, we identified a number of genes that have not previously been implicated in E2 repression, including the demethylase JARID1C/SMCX as well as EP400, a component of the NuA4/TIP60 histone acetyltransferase complex. Each of these genes contributes independently and additively to E2-mediated silencing, indicating that E2 functions through several distinct cellular complexes to repress E6 and E7 expression. View Phenotypes Download PubMed Screen Details Stable ID: GR00197-A-1 Screen Title: Human papillomavirus oncogene expression regulation (1) Assay: HPV18 LCR reporter activity Method: Luminescence Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: C33A/BE2/18LCR c4 Library: Dharmacon, Human siGENOME SMARTpool library Reagent Type: siRNA Score Type: Z-score Cutoff: >= 2 Notes: Author-submitted data; Phenotype strength according to Z-scores: weak: 2 - 3; moderate: 3 - 5; strong: > 5
Cell cycle		PHKG2	shPHKG2-211	0,2	Decreased mitotic index	no
Reference A lentiviral RNAi library for human and mouse genes applied to an arrayed viral high-content screen. Moffat et al., 2006 To enable arrayed or pooled loss-of-function screens in a wide range of mammalian cell types, including primary and nondividing cells, we are developing lentiviral short hairpin RNA (shRNA) libraries targeting the human and murine genomes. The libraries currently contain 104,000 vectors, targeting each of 22,000 human and mouse genes with multiple sequence-verified constructs. To test the utility of the library for arrayed screens, we developed a screen based on high-content imaging to identify genes required for mitotic progression in human cancer cells and applied it to an arrayed set of 5,000 unique shRNA-expressing lentiviruses that target 1,028 human genes. The screen identified several known and approximately 100 candidate regulators of mitotic progression and proliferation; the availability of multiple shRNAs targeting the same gene facilitated functional validation of putative hits. This work provides a widely applicable resource for loss-of-function screens, as well as a roadmap for its application to biological discovery. View Phenotypes Download PubMed Screen Details Stable ID: GR00110-A-0 Screen Title: Cell cycle Assay: Mitotic index Method: High content (microscopy) Scope: Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: HT29 (colon cancer) Library: , TRC shRNA library Reagent Type: shRNA Score Type: Mitotic index Cutoff: >=14 / <= 0.3 Notes:
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000055433	-0,65	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000000399	-0,43	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000010065	1,53	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000010068	-0,99	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000010069	-0,75	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (3)		PHKG2	TRCN0000010069	-0,72	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-3 Screen Title: Proliferation of cells with active beta-catenin (3) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-453 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000010056	0,01	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (1)		PHKG2	TRCN0000000401	0,12	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-1 Screen Title: Proliferation of cells with active beta-catenin (1) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MCF7 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000000401	-0,61	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Wnt/beta-catenin pathway regulation	5261	PHKG2	np	0,93	none	no
Reference Bruton's tyrosine kinase revealed as a negative regulator of Wnt-beta-catenin signaling. James et al., 2009 Wnts are secreted ligands that activate several receptor-mediated signal transduction cascades. Homeostatic Wnt signaling through beta-catenin is required in adults, because either elevation or attenuation of beta-catenin function has been linked to diverse diseases. To contribute to the identification of both protein and pharmacological regulators of this pathway, we describe a combinatorial screen that merged data from a high-throughput screen of known bioactive compounds with an independent focused small interfering RNA screen. Each screen independently revealed Bruton''s tyrosine kinase (BTK) as an inhibitor of Wnt-beta-catenin signaling. Loss of BTK function in human colorectal cancer cells, human B cells, zebrafish embryos, and cells derived from X-linked agammaglobulinemia patients with a mutant BTK gene resulted in elevated Wnt-beta-catenin signaling, confirming that BTK acts as a negative regulator of this pathway. From affinity purification-mass spectrometry and biochemical binding studies, we found that BTK directly interacts with a nuclear component of Wnt-beta-catenin signaling, CDC73. Further, we show that BTK increased the abundance of CDC73 in the absence of stimulation and that CDC73 acted as a repressor of beta-catenin-mediated transcription in human colorectal cancer cells and B cells. View Phenotypes Download PubMed Screen Details Stable ID: GR00016-A Screen Title: Wnt/beta-catenin pathway regulation Assay: Wnt/beta-catenin pathway reporter Method: Luminescence Scope: Selected genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: RKO Library: rp, rp Reagent Type: siRNA Score Type: Z-score Cutoff: > 2 Notes:
Proliferation of cells with active beta-catenin (4)		PHKG2	TRCN0000000401	-0,46	none	no
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-4 Screen Title: Proliferation of cells with active beta-catenin (4) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: T47D Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000000398	0,23	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Genome stability	NM_000294	PHKG2	np	sp	none	no
Reference A genome-wide siRNA screen reveals diverse cellular processes and pathways that mediate genome stability. Paulsen et al., 2009 Signaling pathways that respond to DNA damage are essential for the maintenance of genome stability and are linked to many diseases, including cancer. Here, a genome-wide siRNA screen was employed to identify additional genes involved in genome stabilization by monitoring phosphorylation of the histone variant H2AX, an early mark of DNA damage. We identified hundreds of genes whose downregulation led to elevated levels of H2AX phosphorylation (gammaH2AX) and revealed links to cellular complexes and to genes with unclassified functions. We demonstrate a widespread role for mRNA-processing factors in preventing DNA damage, which in some cases is caused by aberrant RNA-DNA structures. Furthermore, we connect increased gammaH2AX levels to the neurological disorder Charcot-Marie-Tooth (CMT) syndrome, and we find a role for several CMT proteins in the DNA-damage response. These data indicate that preservation of genome stability is mediated by a larger network of biological processes than previously appreciated. View Phenotypes Download PubMed Screen Details Stable ID: GR00053-A Screen Title: Genome stability Assay: gamma-H2AX phosphorylation and DNA content Method: Fluorescence Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: HeLa Library: ThermoFisher Scientiﬁc, siARRAY human genome siRNA library Reagent Type: siRNA Score Type: p-value Cutoff: Complex criteria Notes: Confidence groupings from 4 to 1 (highest level of confidence in group 4)
Therapeutic kinase targets in neuroblastoma (2)	5261	PHKG2	PHKG2	np	none	yes
Reference RNAi screen of the protein kinome identifies checkpoint kinase 1 (CHK1) as a therapeutic target in neuroblastoma. Cole et al., 2011 Neuroblastoma is a childhood cancer that is often fatal despite intense multimodality therapy. In an effort to identify therapeutic targets for this disease, we performed a comprehensive loss-of-function screen of the protein kinome. Thirty kinases showed significant cellular cytotoxicity when depleted, with loss of the cell cycle checkpoint kinase 1 (CHK1/CHEK1) being the most potent. CHK1 mRNA expression was higher in MYC-Neuroblastoma-related (MYCN)-amplified (P < 0.0001) and high-risk (P = 0.03) tumors. Western blotting revealed that CHK1 was constitutively phosphorylated at the ataxia telangiectasia response kinase target site Ser345 and the autophosphorylation site Ser296 in neuroblastoma cell lines. This pattern was also seen in six of eight high-risk primary tumors but not in control nonneuroblastoma cell lines or in seven of eight low-risk primary tumors. Neuroblastoma cells were sensitive to the two CHK1 inhibitors SB21807 and TCS2312, with median IC(50) values of 564 nM and 548 nM, respectively. In contrast, the control lines had high micromolar IC(50) values, indicating a strong correlation between CHK1 phosphorylation and CHK1 inhibitor sensitivity (P = 0.0004). Furthermore, cell cycle analysis revealed that CHK1 inhibition in neuroblastoma cells caused apoptosis during S-phase, consistent with its role in replication fork progression. CHK1 inhibitor sensitivity correlated with total MYC(N) protein levels, and inducing MYCN in retinal pigmented epithelial cells resulted in CHK1 phosphorylation, which caused growth inhibition when inhibited. These data show the power of a functional RNAi screen to identify tractable therapeutical targets in neuroblastoma and support CHK1 inhibition strategies in this disease. View Phenotypes Download PubMed Screen Details Stable ID: GR00193-A-2 Screen Title: Therapeutic kinase targets in neuroblastoma (2) Assay: Substrate adherent cell growth Method: rp Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: KELLY Library: Thermo Scientific, Kinase siGenome library Reagent Type: siRNA Score Type: Relative growth Cutoff: 0.5 standard deviations below mean Notes:
tau phosphorylation		PHKG2	PHKG2 s1	sp	none	no
Reference High-content siRNA screening of the kinome identifies kinases involved in Alzheimer's disease-related tau hyperphosphorylation. Azorsa et al., 2010 Neurofibrillary tangles (NFT), a cardinal neuropathological feature of Alzheimer''s disease (AD) that is highly correlated with synaptic loss and dementia severity, appear to be partly attributable to increased phosphorylation of the microtubule stabilizing protein tau at certain AD-related residues. Identifying the kinases involved in the pathologic phosphorylation of tau may provide targets at which to aim new AD-modifying treatments. View Phenotypes Download PubMed Screen Details Stable ID: GR00143-A Screen Title: tau phosphorylation Assay: Total tau and 12E8 tau protein expression Method: Fluorescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: H4 overexpressing 4RON tau Library: Qiagen, Validated human kinase siRNA Set 2.0 Reagent Type: siRNA Score Type: p-value Cutoff: Complex criteria Notes:
Ciliogenesis and cilium length (1)	5261	PHKG2	289133	42,34	none	no
Reference Functional genomic screen for modulators of ciliogenesis and cilium length. Kim et al., 2010 Primary cilia are evolutionarily conserved cellular organelles that organize diverse signalling pathways. Defects in the formation or function of primary cilia are associated with a spectrum of human diseases and developmental abnormalities. Genetic screens in model organisms have discovered core machineries of cilium assembly and maintenance. However, regulatory molecules that coordinate the biogenesis of primary cilia with other cellular processes, including cytoskeletal organization, vesicle trafficking and cell-cell adhesion, remain to be identified. Here we report the results of a functional genomic screen using RNA interference (RNAi) to identify human genes involved in ciliogenesis control. The screen identified 36 positive and 13 negative ciliogenesis modulators, which include molecules involved in actin dynamics and vesicle trafficking. Further investigation demonstrated that blocking actin assembly facilitates ciliogenesis by stabilizing the pericentrosomal preciliary compartment (PPC), a previously uncharacterized compact vesiculotubular structure storing transmembrane proteins destined for cilia during the early phase of ciliogenesis. The PPC was labelled by recycling endosome markers. Moreover, knockdown of modulators that are involved in the endocytic recycling pathway affected the formation of the PPC as well as ciliogenesis. Our results uncover a critical regulatory step that couples actin dynamics and endocytic recycling with ciliogenesis, and also provides potential target molecules for future study. View Phenotypes Download PubMed Screen Details Stable ID: GR00149-A-1 Screen Title: Ciliogenesis and cilium length (1) Assay: Smoothed protein expression Method: Fluorescence Scope: Druggable genes Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: htRPE Library: Ambion, Human druggable genome siRNA library V3.1 Reagent Type: siRNA Score Type: Normalized percent inhibition Cutoff: > 1.5 OR < -1.5 standard deviations from mean Notes:
Proliferation of cells with active beta-catenin (2)		PHKG2	TRCN0000010068	-0,62	none	yes
Reference CK1epsilon is required for breast cancers dependent on beta-catenin activity. Kim et al., 2010 Aberrant beta-catenin signaling plays a key role in several cancer types, notably colon, liver and breast cancer. However approaches to modulate beta-catenin activity for therapeutic purposes have proven elusive to date. View Phenotypes Download PubMed Screen Details Stable ID: GR00221-A-2 Screen Title: Proliferation of cells with active beta-catenin (2) Assay: Viability Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MDA-MB-231 Library: The RNAi Consortium (TRC), TRC shRNA Library Reagent Type: shRNA Score Type: B-score Cutoff: < -1 Notes: Essential gene: gene with B-score < -1 for >= 2 shRNAs
Homologous recombination DNA double-strand break repair (HR-DSBR) (1)	ENSG00000156873	PHKG2	np	0,07	none	no
Reference A genome-scale DNA repair RNAi screen identifies SPG48 as a novel gene associated with hereditary spastic paraplegia. Słabicki et al., 2010 DNA repair is essential to maintain genome integrity, and genes with roles in DNA repair are frequently mutated in a variety of human diseases. Repair via homologous recombination typically restores the original DNA sequence without introducing mutations, and a number of genes that are required for homologous recombination DNA double-strand break repair (HR-DSBR) have been identified. However, a systematic analysis of this important DNA repair pathway in mammalian cells has not been reported. Here, we describe a genome-scale endoribonuclease-prepared short interfering RNA (esiRNA) screen for genes involved in DNA double strand break repair. We report 61 genes that influenced the frequency of HR-DSBR and characterize in detail one of the genes that decreased the frequency of HR-DSBR. We show that the gene KIAA0415 encodes a putative helicase that interacts with SPG11 and SPG15, two proteins mutated in hereditary spastic paraplegia (HSP). We identify mutations in HSP patients, discovering KIAA0415/SPG48 as a novel HSP-associated gene, and show that a KIAA0415/SPG48 mutant cell line is more sensitive to DNA damaging drugs. We present the first genome-scale survey of HR-DSBR in mammalian cells providing a dataset that should accelerate the discovery of novel genes with roles in DNA repair and associated medical conditions. The discovery that proteins forming a novel protein complex are required for efficient HR-DSBR and are mutated in patients suffering from HSP suggests a link between HSP and DNA repair. View Phenotypes Download PubMed Screen Details Stable ID: GR00151-A-1 Screen Title: Homologous recombination DNA double-strand break repair (HR-DSBR) (1) Assay: (HR-DSBR) DR-GFP reporter Method: Flow cytometry Scope: Genome-wide Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: HeLa Library: Custom-made, Custom-made Reagent Type: esiRNA Score Type: Z-score Cutoff: < -2 OR > 2 Notes:
Combinatorial effect with gemcitabine		PHKG2	PHKG2_B	-0,94	none	no
Reference Synthetic lethal RNAi screening identifies sensitizing targets for gemcitabine therapy in pancreatic cancer. Azorsa et al., 2009 Pancreatic cancer retains a poor prognosis among the gastrointestinal cancers. It affects 230,000 individuals worldwide, has a very high mortality rate, and remains one of the most challenging malignancies to treat successfully. Treatment with gemcitabine, the most widely used chemotherapeutic against pancreatic cancer, is not curative and resistance may occur. Combinations of gemcitabine with other chemotherapeutic drugs or biological agents have resulted in limited improvement. View Phenotypes Download PubMed Screen Details Stable ID: GR00225-A Screen Title: Combinatorial effect with gemcitabine Assay: Viability (synthetic lethal) Method: Luminescence Scope: Kinases Screen Type: Cell-based Species: Homo sapiens Biosource: Cell line Biomodel: MIA PaCa-2 Library: Qiagen, Validated kinase siRNA library version 1.0 Reagent Type: siRNA Score Type: log2 ratio Cutoff: 1.65 SD below mean ratio level Notes:

Reagent information for gene 5261 (PHKG2)

Reagent ID	Type	Library
TRCN0000196825	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000055433	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000000400	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000010069	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000196908	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000000401	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000010068	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000122476	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000130998	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000010065	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000000398	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000129540	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000195430	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000148796	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000010056	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000000399	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000129610	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000199678	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
TRCN0000199891	shRNA	TRC shRNA Library\|The RNAi Consortium (TRC)\|1\|RefSeq\|81054\|shRNA\|http://www.broadinstitute.org/rnai/public/
D-030737-03	siRNA	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
D-004881-04	siRNA	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
D-004881-03	siRNA	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
D-004881-01	siRNA	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
D-004881-02	siRNA	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
D-030737-04	siRNA	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
D-030737-02	siRNA	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
D-030737-01	siRNA	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
SI00006391	siRNA	Druggable and whole genome supplement\|Qiagen\|1, 3\|RefSeq\|70308 siRNAs in pools of four\|siRNA\|http://www.qiagen.com/
SI00604884	siRNA	Druggable and whole genome supplement\|Qiagen\|1, 3\|RefSeq\|70308 siRNAs in pools of four\|siRNA\|http://www.qiagen.com/
SI00006405	siRNA	Druggable and whole genome supplement\|Qiagen\|1, 3\|RefSeq\|70308 siRNAs in pools of four\|siRNA\|http://www.qiagen.com/
SI00604891	siRNA	Druggable and whole genome supplement\|Qiagen\|1, 3\|RefSeq\|70308 siRNAs in pools of four\|siRNA\|http://www.qiagen.com/
s10451	siRNA	Ambion Silencer Select\|Ambion\|1\|RefSeq\|64781\|siRNA\|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
s10452	siRNA	Ambion Silencer Select\|Ambion\|1\|RefSeq\|64781\|siRNA\|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
s10453	siRNA	Ambion Silencer Select\|Ambion\|1\|RefSeq\|64781\|siRNA\|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
s40503	siRNA	Ambion Silencer Select\|Ambion\|1\|RefSeq\|64781\|siRNA\|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
s57083	siRNA	Ambion Silencer Select\|Ambion\|1\|RefSeq\|64781\|siRNA\|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
s57084	siRNA	Ambion Silencer Select\|Ambion\|1\|RefSeq\|64781\|siRNA\|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
s40505	siRNA	Ambion Silencer Select\|Ambion\|1\|RefSeq\|64781\|siRNA\|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
M-030737-00	siRNA_Pool	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
M-004881-00	siRNA_Pool	siGENOME\|Thermo Scientific Dharmacon\|1\|RefSeq release 5-7\|84206 siRNAs in pools of four\|siRNA\|http://www.dharmacon.com/
SP00006475	siRNA_Pool	Druggable and whole genome supplement\|Qiagen\|1, 3\|RefSeq\|70308 siRNAs in pools of four\|siRNA\|http://www.qiagen.com/

Gene information for gene 5261 (PHKG2)

Gene:	PHKG2
Alternate gene names:	GSD9C
Description:	phosphorylase kinase, gamma 2 (testis)
Chromosome:	16
Start:	30759619
Stop:	30772496
Strand:	positive
Locus:	16p11.2
Biotype:	protein-coding
Status:	live
Entrez Gene:	5261
GeneCards:	5261
Ensembl:	ENSG00000156873
Hgnc:	8931
Hprd:	01405
Mim:	172471
Uniprot:	P15735
Vega:	OTTHUMG00000132400
RefSeq:	NM_000294 NM_001172432

Homologs:

Gene	Chromosome	Locus	Organism
PhKgamma	X		Drosophila melanogaster

Genome browser for gene 5261 (PHKG2)

Homo sapiens GRCh37

Dalliance requires a modern Javascript-enabled web browser. If in doubt, please download the latest version of Firefox, Google Chrome, or Safari for your platform.

human

http://genomernai.de/DASGenomeRNAi/das/

http://www.derkholm.net:8080/das/hsa_59_37d/

http://www.derkholm.net:8080/das/dme_61_525c/

GRCh

BDGP

30759619

30772496

http://genomernai.de:8010/rnaiseq_binary

Phenotype information for gene 5261 (PHKG2)

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details

Reference

Screen Details