BAIT
BMI1
FLVI2/BMI1, PCGF4, RNF51, RP11-573G6.1
BMI1 proto-oncogene, polycomb ring finger
GO Process (6)
GO Function (3)
GO Component (5)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
TSC2
LAM, PPP1R160, TSC4
tuberous sclerosis 2
GO Process (28)
GO Function (4)
GO Component (7)
Gene Ontology Biological Process
- Fc-epsilon receptor signaling pathway [TAS]
- cell cycle arrest [TAS]
- endocytosis [TAS]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- heart development [ISS]
- innate immune response [TAS]
- insulin receptor signaling pathway [TAS]
- insulin-like growth factor receptor signaling pathway [ISS]
- negative regulation of TOR signaling [IBA]
- negative regulation of Wnt signaling pathway [IBA]
- negative regulation of cell proliferation [ISS]
- negative regulation of insulin receptor signaling pathway [IBA]
- negative regulation of phosphatidylinositol 3-kinase signaling [ISS]
- negative regulation of protein kinase B signaling [IBA, ISS]
- negative regulation of protein kinase activity [ISS]
- neural tube closure [ISS]
- neurotrophin TRK receptor signaling pathway [TAS]
- phosphatidylinositol-mediated signaling [TAS]
- positive chemotaxis [ISS]
- positive regulation of Ras GTPase activity [IBA]
- protein import into nucleus [ISS]
- protein kinase B signaling [ISS]
- protein localization [ISS]
- regulation of cell cycle [IBA]
- regulation of endocytosis [ISS]
- regulation of insulin receptor signaling pathway [ISS]
- vesicle-mediated transport [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
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
Synergistic drug combinations for cancer identified in a CRISPR screen for pairwise genetic interactions.
Identification of effective combination therapies is critical to address the emergence of drug-resistant cancers, but direct screening of all possible drug combinations is infeasible. Here we introduce a CRISPR-based double knockout (CDKO) system that improves the efficiency of combinatorial genetic screening using an effective strategy for cloning and sequencing paired single guide RNA (sgRNA) libraries and a robust statistical scoring ... [more]
Nat. Biotechnol. Mar. 20, 2017; 0(); [Pubmed: 28319085]
Quantitative Score
- -2.236 [Confidence Score]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507)
Additional Notes
- CRISPR GI screen
- Cell Line:K562 (EFO:0002067)
- Experimental Setup:Toxin Exposure: Ricin at LD50 (first two pulses: 0.25 ng/ml ricin, third pulse: 0.3 ng/ml, fourth pulse: 0.35 ng/ml)
- GIST: A-phenotypic negative genetic interaction
- Library:Ricin-CDKO CRISPRn library
- Significance Threshold: q-value<0.05
Curated By
- BioGRID