BAIT
CFLAR
CASH, CASP8AP1, CLARP, Casper, FLAME, FLAME-1, FLAME1, FLIP, I-FLICE, MRIT, c-FLIP, c-FLIPL, c-FLIPR, c-FLIPS
CASP8 and FADD-like apoptosis regulator
GO Process (16)
GO Function (5)
GO Component (4)
Gene Ontology Biological Process
- apoptotic process [IMP, TAS]
- apoptotic signaling pathway [TAS]
- negative regulation of apoptotic process [TAS]
- negative regulation of extrinsic apoptotic signaling pathway [IDA, IMP]
- negative regulation of extrinsic apoptotic signaling pathway via death domain receptors [IMP]
- negative regulation of myoblast fusion [ISS]
- positive regulation of I-kappaB kinase/NF-kappaB signaling [IEP]
- positive regulation of NF-kappaB transcription factor activity [ISS]
- positive regulation of catalytic activity [IDA]
- regulation of extrinsic apoptotic signaling pathway in absence of ligand [TAS]
- regulation of necroptotic process [IDA]
- regulation of satellite cell proliferation [ISS]
- skeletal muscle atrophy [ISS]
- skeletal muscle tissue development [ISS]
- skeletal muscle tissue regeneration [ISS]
- skeletal myofibril assembly [ISS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
TNFRSF1A
CD120a, FPF, MS5, TBP1, TNF-R, TNF-R-I, TNF-R55, TNFAR, TNFR1, TNFR1-d2, TNFR55, TNFR60, p55, p55-R, p60
tumor necrosis factor receptor superfamily, member 1A
GO Process (11)
GO Function (2)
GO Component (7)
Gene Ontology Biological Process
- apoptotic process [TAS]
- apoptotic signaling pathway [TAS]
- cellular response to mechanical stimulus [IEP]
- cytokine-mediated signaling pathway [ISS]
- extrinsic apoptotic signaling pathway via death domain receptors [TAS]
- inflammatory response [ISS]
- negative regulation of inflammatory response [IMP]
- positive regulation of I-kappaB kinase/NF-kappaB signaling [IEP]
- positive regulation of inflammatory response [ISS]
- positive regulation of transcription from RNA polymerase II promoter [IMP, ISS]
- positive regulation of tyrosine phosphorylation of Stat1 protein [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Phenotypic Suppression
A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.
Publication
CRISPR/Cas9 Screens Reveal Epstein-Barr Virus-Transformed B Cell Host Dependency Factors.
Epstein-Barr virus (EBV) causes endemic Burkitt lymphoma (BL) and immunosuppression-related lymphomas. These B cell malignancies arise by distinct transformation pathways and have divergent viral and host expression programs. To identify host dependency factors resulting from these EBV+, B cell-transformed cell states, we performed parallel genome-wide CRISPR/Cas9 loss-of-function screens in BL and lymphoblastoid cell lines (LCLs). These highlighted 57 BL and 87 LCL ... [more]
Cell Host Microbe May. 10, 2017; 21(5);580-591.e7 [Pubmed: 28494239]
Throughput
- Low Throughput
Ontology Terms
- phenotype: viability (APO:0000111)
Additional Notes
- sgRNAs targeting TNFRSF1A rescued LCLs from CFLAR dependency
Curated By
- BioGRID