BCL2L1
Gene Ontology Biological Process
- apoptotic mitochondrial changes [TAS]
- apoptotic process [TAS]
- cytokinesis [IMP]
- extrinsic apoptotic signaling pathway in absence of ligand [IBA]
- innate immune response [TAS]
- intrinsic apoptotic signaling pathway [TAS]
- mitotic cell cycle checkpoint [IMP]
- negative regulation of anoikis [IMP]
- negative regulation of apoptotic process [IDA, IMP]
- negative regulation of autophagy [TAS]
- negative regulation of establishment of protein localization to plasma membrane [IDA]
- negative regulation of execution phase of apoptosis [IDA]
- negative regulation of extrinsic apoptotic signaling pathway in absence of ligand [TAS]
- negative regulation of intrinsic apoptotic signaling pathway [IDA]
- negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage [IDA]
- negative regulation of release of cytochrome c from mitochondria [IC, IDA]
- nucleotide-binding domain, leucine rich repeat containing receptor signaling pathway [TAS]
- positive regulation of intrinsic apoptotic signaling pathway [TAS]
- regulation of mitochondrial membrane permeability [IDA]
- regulation of mitochondrial membrane potential [IDA]
- release of cytochrome c from mitochondria [IDA]
- response to cytokine [IDA]
- suppression by virus of host apoptotic process [IDA]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
BCL2L2
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Negative Genetic
Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.
Publication
Paralog knockout profiling identifies DUSP4 and DUSP6 as a digenic dependence in MAPK pathway-driven cancers.
Although single-gene perturbation screens have revealed a number of new targets, vulnerabilities specific to frequently altered drivers have not been uncovered. An important question is whether the compensatory relationship between functionally redundant genes masks potential therapeutic targets in single-gene perturbation studies. To identify digenic dependencies, we developed a CRISPR paralog targeting library to investigate the viability effects of disrupting 3,284 ... [more]
Quantitative Score
- 0.040313476 [Confidence Score]
Throughput
- High Throughput
Additional Notes
- CRISPR GI screen
- Cell Line: MELJUSO_SKIN score (1.28348936092513E-06)
- Cell Line: PK1_PANCREAS score (0.0001168133985715)
- Cell Line: GI1_CENTRAL_NERVOUS_SYSTEM score (0.0403134756947631)
- Cell Line: HS944T_SKIN score (1.4417321415676E-13)
- Cell Line: HSC5_SKIN score (0.0350059153343443)
- Experimental Setup: Timecourse-Synthetic Lethality
- GIST: A-phenotypic negative genetic interaction
- Library: Digenic Paralog CRISPR library
- Significance Threshold: GEMINI FDR < 0.05
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| BCL2L1 BCL2L2 | Negative Genetic Negative Genetic Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores. | High | -3.354 | BioGRID | 2538062 |
Curated By
- BioGRID