BAIT
ATM
AT1, ATA, ATC, ATD, ATDC, ATE, TEL1, TELO1
ATM serine/threonine kinase
GO Process (23)
GO Function (7)
GO Component (2)
Gene Ontology Biological Process
- DNA damage induced protein phosphorylation [IDA]
- DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest [TAS]
- DNA repair [TAS]
- cell cycle arrest [IMP]
- cellular response to DNA damage stimulus [IMP]
- cellular response to gamma radiation [IDA]
- double-strand break repair [TAS]
- double-strand break repair via homologous recombination [TAS]
- histone mRNA catabolic process [IDA]
- mitotic spindle assembly checkpoint [IMP]
- negative regulation of B cell proliferation [IMP]
- peptidyl-serine phosphorylation [IDA]
- phosphatidylinositol-3-phosphate biosynthetic process [IMP]
- positive regulation of DNA damage response, signal transduction by p53 class mediator [IMP]
- positive regulation of apoptotic process [IMP]
- pre-B cell allelic exclusion [ISS]
- protein autophosphorylation [IDA]
- protein phosphorylation [IDA]
- reciprocal meiotic recombination [TAS]
- replicative senescence [IMP]
- response to ionizing radiation [IDA]
- signal transduction [TAS]
- signal transduction involved in mitotic G2 DNA damage checkpoint [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
MAP3K4
MAPKKK4, MEKK 4, MEKK4, MTK1, PRO0412, RP3-473J16.4
mitogen-activated protein kinase kinase kinase 4
GO Process (6)
GO Function (2)
GO Component (1)
Gene Ontology Biological Process
Gene Ontology Molecular Function
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
- -4.301 [Confidence Score]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507)
Additional Notes
- CRISPR GI screen
- Cell Line:K562 (EFO:0002067)
- Experimental Setup:Timecourse
- GIST: A-phenotypic negative genetic interaction
- Library:Drug Target-CDKO CRISPRn library
- Significance Threshold: q-value<0.05
Curated By
- BioGRID