GenomeRNAi - a database for RNAi phenotypes and reagents

Phenotype information for gene 94025 (MUC16)

Screen TitleGene IDGene SymbolReagent IDScorePhenotypeComment
TRAIL-induced apoptosis (2)
NM_003941
WASL
-0.57
none Z-score -0.764

Reference

A synthetic lethal screen identifies FAT1 as an antagonist of caspase-8 in extrinsic apoptosis. Kranz and Boutros, 2014

The extrinsic apoptosis pathway is initiated by binding of death ligands to death receptors resulting in the formation of the death-inducing signaling complex (DISC). Activation of procaspase-8 within the DISC and its release from the signaling complex is required for processing executor caspases and commiting cell death. Here, we report that the atypical cadherin FAT1 interacts with caspase-8 preventing the association of caspase-8 with the DISC. We identified FAT1 in a genome-wide siRNA screen for synthetic lethal interactions with death receptor-mediated apoptosis. Knockdown of FAT1 sensitized established and patient-derived glioblastoma cell lines for apoptosis transduced by cell death ligands. Depletion of FAT1 resulted in enhanced procaspase-8 recruitment to the DISC and increased formation of caspase-8 containing secondary signaling complexes. In addition, FAT1 knockout cell lines generated by CRISPR/Cas9-mediated genome engineering were more susceptible for death receptor-mediated apoptosis. Our findings provide evidence for a mechanism to control caspase-8-dependent cell death by the atypical cadherin FAT1. These results contribute towards the understanding of effector caspase regulation in physiological conditions.

Screen Details

Stable ID: GR00240-S-2
Screen Title: TRAIL-induced apoptosis (2)
Assay: Viability (synthetic lethal)
Method: Luminescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: U251MG
Library: Dharmacon, SMART-pool siRNA
Reagent Type: siRNA
Score Type: Differential score
Cutoff: > 3.6 AND viability Z-score < 4
Notes: Author-submitted data. Z-scores from viability screen (1) are considered in score interpretation for this screen.

Human papillomavirus oncogene expression regulation (1)
8976
WASL
-0.31
none

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.

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

Vaccinia virus (VACV) infection
94025
MUC16
M-032591-01
1.61
Increased vaccinia virus (VACV) infection number of cells compared to control (%): 72.58

Reference

Human genome-wide RNAi screen reveals a role for nuclear pore proteins in poxvirus morphogenesis. Sivan et al., 2013

Poxviruses are considered less dependent on host functions than other DNA viruses because of their cytoplasmic site of replication and large genomes, which encode enzymes for DNA and mRNA synthesis. Nevertheless, RNAi screens with two independent human genome-scale libraries have identified more than 500 candidate genes that significantly inhibited and a similar number that enhanced replication and spread of infectious vaccinia virus (VACV). Translational, ubiquitin-proteosome, and endoplasmic reticulum-to-Golgi transport functions, known to be important for VACV, were enriched in the siRNA-inhibiting group, and RNA polymerase II and associated functions were enriched in the siRNA-enhancing group. Additional findings, notably the inhibition of VACV spread by siRNAs to several nuclear pore genes, were unanticipated. Knockdown of nucleoporin 62 strongly inhibited viral morphogenesis, with only a modest effect on viral gene expression, recapitulating and providing insight into previous studies with enucleated cells.

Screen Details

Stable ID: GR00249-S
Screen Title: Vaccinia virus (VACV) infection
Assay: Vaccinia virus VACV IHD-J/GFP protein expression and DNA content
Method: Fluorescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: HeLa
Library: Ambion and Dharmacon, Silencer Select Version 4, siGENOME SMARTpool and OnTargetPlus
Reagent Type: siRNA
Score Type: Z-score
Cutoff: >= 1 OR <= -1.5
Notes: Author-submitted data. Primary screen. Decreased viability phenotype if number of cells compared to control < 50 %.

Vaccinia virus (VACV) infection
94025
MUC16
-0.5
none number of cells compared to control (%): 85.58

Reference

Human genome-wide RNAi screen reveals a role for nuclear pore proteins in poxvirus morphogenesis. Sivan et al., 2013

Poxviruses are considered less dependent on host functions than other DNA viruses because of their cytoplasmic site of replication and large genomes, which encode enzymes for DNA and mRNA synthesis. Nevertheless, RNAi screens with two independent human genome-scale libraries have identified more than 500 candidate genes that significantly inhibited and a similar number that enhanced replication and spread of infectious vaccinia virus (VACV). Translational, ubiquitin-proteosome, and endoplasmic reticulum-to-Golgi transport functions, known to be important for VACV, were enriched in the siRNA-inhibiting group, and RNA polymerase II and associated functions were enriched in the siRNA-enhancing group. Additional findings, notably the inhibition of VACV spread by siRNAs to several nuclear pore genes, were unanticipated. Knockdown of nucleoporin 62 strongly inhibited viral morphogenesis, with only a modest effect on viral gene expression, recapitulating and providing insight into previous studies with enucleated cells.

Screen Details

Stable ID: GR00249-S
Screen Title: Vaccinia virus (VACV) infection
Assay: Vaccinia virus VACV IHD-J/GFP protein expression and DNA content
Method: Fluorescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: HeLa
Library: Ambion and Dharmacon, Silencer Select Version 4, siGENOME SMARTpool and OnTargetPlus
Reagent Type: siRNA
Score Type: Z-score
Cutoff: >= 1 OR <= -1.5
Notes: Author-submitted data. Primary screen. Decreased viability phenotype if number of cells compared to control < 50 %.

Vaccinia virus (VACV) infection
94025
MUC16
J-032591-09
-0.56
none number of cells compared to control (%): 62.25

Reference

Human genome-wide RNAi screen reveals a role for nuclear pore proteins in poxvirus morphogenesis. Sivan et al., 2013

Poxviruses are considered less dependent on host functions than other DNA viruses because of their cytoplasmic site of replication and large genomes, which encode enzymes for DNA and mRNA synthesis. Nevertheless, RNAi screens with two independent human genome-scale libraries have identified more than 500 candidate genes that significantly inhibited and a similar number that enhanced replication and spread of infectious vaccinia virus (VACV). Translational, ubiquitin-proteosome, and endoplasmic reticulum-to-Golgi transport functions, known to be important for VACV, were enriched in the siRNA-inhibiting group, and RNA polymerase II and associated functions were enriched in the siRNA-enhancing group. Additional findings, notably the inhibition of VACV spread by siRNAs to several nuclear pore genes, were unanticipated. Knockdown of nucleoporin 62 strongly inhibited viral morphogenesis, with only a modest effect on viral gene expression, recapitulating and providing insight into previous studies with enucleated cells.

Screen Details

Stable ID: GR00249-S
Screen Title: Vaccinia virus (VACV) infection
Assay: Vaccinia virus VACV IHD-J/GFP protein expression and DNA content
Method: Fluorescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: HeLa
Library: Ambion and Dharmacon, Silencer Select Version 4, siGENOME SMARTpool and OnTargetPlus
Reagent Type: siRNA
Score Type: Z-score
Cutoff: >= 1 OR <= -1.5
Notes: Author-submitted data. Primary screen. Decreased viability phenotype if number of cells compared to control < 50 %.

TRAIL-induced apoptosis (1)
NM_003941
WASL
-0.28
none

Reference

A synthetic lethal screen identifies FAT1 as an antagonist of caspase-8 in extrinsic apoptosis. Kranz and Boutros, 2014

The extrinsic apoptosis pathway is initiated by binding of death ligands to death receptors resulting in the formation of the death-inducing signaling complex (DISC). Activation of procaspase-8 within the DISC and its release from the signaling complex is required for processing executor caspases and commiting cell death. Here, we report that the atypical cadherin FAT1 interacts with caspase-8 preventing the association of caspase-8 with the DISC. We identified FAT1 in a genome-wide siRNA screen for synthetic lethal interactions with death receptor-mediated apoptosis. Knockdown of FAT1 sensitized established and patient-derived glioblastoma cell lines for apoptosis transduced by cell death ligands. Depletion of FAT1 resulted in enhanced procaspase-8 recruitment to the DISC and increased formation of caspase-8 containing secondary signaling complexes. In addition, FAT1 knockout cell lines generated by CRISPR/Cas9-mediated genome engineering were more susceptible for death receptor-mediated apoptosis. Our findings provide evidence for a mechanism to control caspase-8-dependent cell death by the atypical cadherin FAT1. These results contribute towards the understanding of effector caspase regulation in physiological conditions.

Screen Details

Stable ID: GR00240-S-1
Screen Title: TRAIL-induced apoptosis (1)
Assay: Viability
Method: Luminescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: U251MG
Library: Dharmacon, SMART-pool siRNA
Reagent Type: siRNA
Score Type: Z-score
Cutoff: > 4
Notes: Author-submitted data

TP53 interactions (1)
ENSG00000181143
np
sp
none

Reference

A systematic RNAi synthetic interaction screen reveals a link between p53 and snoRNP assembly. Krastev et al., 2011

TP53 (tumour protein 53) is one of the most frequently mutated genes in human cancer and its role during cellular transformation has been studied extensively. However, the homeostatic functions of p53 are less well understood. Here, we explore the molecular dependency network of TP53 through an RNAi-mediated synthetic interaction screen employing two HCT116 isogenic cell lines and a genome-scale endoribonuclease-prepared short interfering RNA library. We identify a variety of TP53 synthetic interactions unmasking the complex connections of p53 to cellular physiology and growth control. Molecular dissection of the TP53 synthetic interaction with UNRIP indicates an enhanced dependency of TP53-negative cells on small nucleolar ribonucleoprotein (snoRNP) assembly. This dependency is mediated by the snoRNP chaperone gene NOLC1 (also known as NOPP140), which we identify as a physiological p53 target gene. This unanticipated function of TP53 in snoRNP assembly highlights the potential of RNAi-mediated synthetic interaction screens to dissect molecular pathways of tumour suppressor genes.

Screen Details

Stable ID: GR00196-A-1
Screen Title: TP53 interactions (1)
Assay: TP53 protein expression and viability
Method: Fluorescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: HCT116 ( wildtype and TP53 knockout)
Library: Custom-made, rp
Reagent Type: esiRNA
Score Type: Complex, sp
Cutoff: Complex criteria
Notes:

Homologous recombination DNA double-strand break repair (HR-DSBR) (1)
ENSG00000181143
MUC16
np
1.26
none

Reference

A genome-scale DNA repair RNAi screen identifies SPG48 as a novel gene associated with hereditary spastic paraplegia. SÅ‚abicki 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.

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:

Homologous recombination DNA double-strand break repair (HR-DSBR) (1)
8976
WASL
0.84
none

Reference

A genome-wide homologous recombination screen identifies the RNA-binding protein RBMX as a component of the DNA-damage response. Adamson et al., 2012

Repair of DNA double-strand breaks is critical to genomic stability and the prevention of developmental disorders and cancer. A central pathway for this repair is homologous recombination (HR). Most knowledge of HR is derived from work in prokaryotic and eukaryotic model organisms. We carried out a genome-wide siRNA-based screen in human cells. Among positive regulators of HR we identified networks of DNA-damage-response and pre-mRNA-processing proteins, and among negative regulators we identified a phosphatase network. Three candidate proteins localized to DNA lesions, including RBMX, a heterogeneous nuclear ribonucleoprotein that has a role in alternative splicing. RBMX accumulated at DNA lesions through multiple domains in a poly(ADP-ribose) polymerase 1-dependent manner and promoted HR by facilitating proper BRCA2 expression. Our screen also revealed that off-target depletion of RAD51 is a common source of RNAi false positives, raising a cautionary note for siRNA screens and RNAi-based studies of HR.

Screen Details

Stable ID: GR00236-A-1
Screen Title: Homologous recombination DNA double-strand break repair (HR-DSBR) (1)
Assay: (HR-DSBR) DR-GFP reporter and DNA content
Method: Fluorescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: DR-U2OS
Library: Dharmacon, Human siGENOME siRNA (G-005000-05)
Reagent Type: siRNA
Score Type: Relative HR ratio
Cutoff: < ~0.4 OR > 1.88
Notes: Cutoff values correspond 2 standard deviations from the screen-wide mean

Wnt/beta-catenin pathway regulation (1)
NM_003941
WASL
-0.74
none

Reference

A genome-wide RNAi screen for Wnt/beta-catenin pathway components identifies unexpected roles for TCF transcription factors in cancer. Tang et al., 2008

The Wnt family of secreted proteins coordinate cell fate decision-making in a broad range of developmental and homeostatic contexts. Corruption of Wnt signal transduction pathways frequently results in degenerative diseases and cancer. We have used an iterative genome-wide screening strategy that employs multiple nonredundant RNAi reagents to identify mammalian genes that participate in Wnt/beta-catenin pathway response. Among the genes that were assigned high confidence scores are two members of the TCF/LEF family of DNA-binding proteins that control the transcriptional output of the pathway. Surprisingly, we found that the presumed cancer-promoting gene TCF7L2 functions instead as a transcriptional repressor that restricts colorectal cancer (CRC) cell growth. Mutations in TCF7L2 identified from cancer genome sequencing efforts abolish its ability to function as a transcriptional regulator and result in increased CRC cell growth. We describe a growth-promoting transcriptional program that is likely activated in CRC tumors with compromised TCF7L2 function. Taken together, the results from our screen and studies focused on members of the TCF/LEF gene family refine our understanding of how aberrant Wnt pathway activation sustains CRC growth.

Screen Details

Stable ID: GR00057-A-1
Screen Title: Wnt/beta-catenin pathway regulation (1)
Assay: Wnt pathway reporter
Method: Luminescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: HeLa
Library: Dharmacon, Human siArray siRNA library
Reagent Type: siRNA
Score Type: Z-score
Cutoff: > 4
Notes: Screen without Wnt3A stimulation. Additional information about secondary screens (Dharmacon and Qiagen libraries).

Cell division (1)
ENSG00000181143
MUC16
ENSG00000181143
sp
none

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.

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:

Vaccinia virus (VACV) infection
94025
MUC16
0.66
none number of cells compared to control (%): 68.24

Reference

Human genome-wide RNAi screen reveals a role for nuclear pore proteins in poxvirus morphogenesis. Sivan et al., 2013

Poxviruses are considered less dependent on host functions than other DNA viruses because of their cytoplasmic site of replication and large genomes, which encode enzymes for DNA and mRNA synthesis. Nevertheless, RNAi screens with two independent human genome-scale libraries have identified more than 500 candidate genes that significantly inhibited and a similar number that enhanced replication and spread of infectious vaccinia virus (VACV). Translational, ubiquitin-proteosome, and endoplasmic reticulum-to-Golgi transport functions, known to be important for VACV, were enriched in the siRNA-inhibiting group, and RNA polymerase II and associated functions were enriched in the siRNA-enhancing group. Additional findings, notably the inhibition of VACV spread by siRNAs to several nuclear pore genes, were unanticipated. Knockdown of nucleoporin 62 strongly inhibited viral morphogenesis, with only a modest effect on viral gene expression, recapitulating and providing insight into previous studies with enucleated cells.

Screen Details

Stable ID: GR00249-S
Screen Title: Vaccinia virus (VACV) infection
Assay: Vaccinia virus VACV IHD-J/GFP protein expression and DNA content
Method: Fluorescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: HeLa
Library: Ambion and Dharmacon, Silencer Select Version 4, siGENOME SMARTpool and OnTargetPlus
Reagent Type: siRNA
Score Type: Z-score
Cutoff: >= 1 OR <= -1.5
Notes: Author-submitted data. Primary screen. Decreased viability phenotype if number of cells compared to control < 50 %.

Self-renewal and pluripotency in human embryonic stem cells (1)
NM_003941
WASL
-1.51
none

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.

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:

Wnt/beta-catenin pathway regulation (2)
NM_003941
WASL
sp
none

Reference

A genome-wide RNAi screen for Wnt/beta-catenin pathway components identifies unexpected roles for TCF transcription factors in cancer. Tang et al., 2008

The Wnt family of secreted proteins coordinate cell fate decision-making in a broad range of developmental and homeostatic contexts. Corruption of Wnt signal transduction pathways frequently results in degenerative diseases and cancer. We have used an iterative genome-wide screening strategy that employs multiple nonredundant RNAi reagents to identify mammalian genes that participate in Wnt/beta-catenin pathway response. Among the genes that were assigned high confidence scores are two members of the TCF/LEF family of DNA-binding proteins that control the transcriptional output of the pathway. Surprisingly, we found that the presumed cancer-promoting gene TCF7L2 functions instead as a transcriptional repressor that restricts colorectal cancer (CRC) cell growth. Mutations in TCF7L2 identified from cancer genome sequencing efforts abolish its ability to function as a transcriptional regulator and result in increased CRC cell growth. We describe a growth-promoting transcriptional program that is likely activated in CRC tumors with compromised TCF7L2 function. Taken together, the results from our screen and studies focused on members of the TCF/LEF gene family refine our understanding of how aberrant Wnt pathway activation sustains CRC growth.

Screen Details

Stable ID: GR00057-A-2
Screen Title: Wnt/beta-catenin pathway regulation (2)
Assay: Wnt pathway reporter
Method: Luminescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: HeLa
Library: Dharmacon, Human siArray siRNA library
Reagent Type: siRNA
Score Type: Complex, SP
Cutoff: Complex criteria
Notes: Screen with Wnt3A stimulation. Additional information about secondary screens (Dharmacon and Qiagen libraries).

Vaccinia virus (VACV) infection
94025
MUC16
1.58
Increased vaccinia virus (VACV) infection number of cells compared to control (%): 52.52

Reference

Human genome-wide RNAi screen reveals a role for nuclear pore proteins in poxvirus morphogenesis. Sivan et al., 2013

Poxviruses are considered less dependent on host functions than other DNA viruses because of their cytoplasmic site of replication and large genomes, which encode enzymes for DNA and mRNA synthesis. Nevertheless, RNAi screens with two independent human genome-scale libraries have identified more than 500 candidate genes that significantly inhibited and a similar number that enhanced replication and spread of infectious vaccinia virus (VACV). Translational, ubiquitin-proteosome, and endoplasmic reticulum-to-Golgi transport functions, known to be important for VACV, were enriched in the siRNA-inhibiting group, and RNA polymerase II and associated functions were enriched in the siRNA-enhancing group. Additional findings, notably the inhibition of VACV spread by siRNAs to several nuclear pore genes, were unanticipated. Knockdown of nucleoporin 62 strongly inhibited viral morphogenesis, with only a modest effect on viral gene expression, recapitulating and providing insight into previous studies with enucleated cells.

Screen Details

Stable ID: GR00249-S
Screen Title: Vaccinia virus (VACV) infection
Assay: Vaccinia virus VACV IHD-J/GFP protein expression and DNA content
Method: Fluorescence
Scope: Genome-wide
Screen Type: Cell-based
Species: Homo sapiens
Biosource: Cell line
Biomodel: HeLa
Library: Ambion and Dharmacon, Silencer Select Version 4, siGENOME SMARTpool and OnTargetPlus
Reagent Type: siRNA
Score Type: Z-score
Cutoff: >= 1 OR <= -1.5
Notes: Author-submitted data. Primary screen. Decreased viability phenotype if number of cells compared to control < 50 %.

Reagent information for gene 94025 (MUC16)

Reagent IDTypeLibrary
M-006444-01 siRNA_Pool
siGENOME|Thermo Scientific Dharmacon|1|RefSeq release 5-7|84206 siRNAs in pools of four|siRNA|http://www.dharmacon.com/
D-006444-05 siRNA
siGENOME|Thermo Scientific Dharmacon|1|RefSeq release 5-7|84206 siRNAs in pools of four|siRNA|http://www.dharmacon.com/
s41225 siRNA
Ambion Silencer Select|Ambion|1|RefSeq|64781|siRNA|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
s41226 siRNA
Ambion Silencer Select|Ambion|1|RefSeq|64781|siRNA|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion
s41227 siRNA
Ambion Silencer Select|Ambion|1|RefSeq|64781|siRNA|http://www.invitrogen.com/site/us/en/home/brands/ambion.html?CID=fl-ambion

Gene information for gene 94025 (MUC16)

Gene:
Alternate gene names:CA125
Description:mucin 16, cell surface associated
Chromosome:19
Start:8848839
Stop:8981341
Strand:negative
Locus:19p13.2
Biotype:protein-coding
Status:live
Entrez Gene:
GeneCards:
Ensembl:
Hgnc:
Mim:
Uniprot:
Vega:
RefSeq:

Genome browser for gene 94025 (MUC16)

Homo sapiens GRCh38
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