BAIT
CSK
c-src tyrosine kinase
GO Process (18)
GO Function (6)
GO Component (5)
Gene Ontology Biological Process
- T cell costimulation [TAS]
- T cell receptor signaling pathway [TAS]
- adherens junction organization [IBA]
- blood coagulation [TAS]
- cell differentiation [IBA]
- cell migration [IBA]
- central nervous system development [IBA]
- epidermal growth factor receptor signaling pathway [TAS]
- innate immune response [IBA]
- morphogenesis of an epithelium [IBA]
- negative regulation of Golgi to plasma membrane protein transport [IDA]
- peptidyl-tyrosine autophosphorylation [IBA]
- platelet activation [TAS]
- protein phosphorylation [TAS]
- regulation of Fc receptor mediated stimulatory signaling pathway [IBA]
- regulation of cell proliferation [IBA]
- regulation of cytokine production [IBA]
- transmembrane receptor protein tyrosine kinase signaling pathway [IBA]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
EPHB2
CAPB, DRT, EK5, EPHT3, ERK, Hek5, PCBC, Tyro5
EPH receptor B2
GO Process (16)
GO Function (3)
GO Component (3)
Gene Ontology Biological Process
- angiogenesis [ISS]
- axon guidance [ISS, TAS]
- axonal fasciculation [ISS]
- commissural neuron axon guidance [ISS]
- corpus callosum development [ISS]
- dendritic spine development [ISS]
- dendritic spine morphogenesis [ISS]
- ephrin receptor signaling pathway [ISS]
- inner ear morphogenesis [ISS]
- nervous system development [TAS]
- palate development [ISS]
- peptidyl-tyrosine phosphorylation [ISS]
- phosphorylation [ISS]
- positive regulation of synapse assembly [ISS]
- regulation of body fluid levels [ISS]
- urogenital system development [ISS]
Gene Ontology Molecular Function
Homo sapiens
Synthetic Lethality
A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.
Publication
Estrogen-regulated feedback loop limits the efficacy of estrogen receptor-targeted breast cancer therapy.
Endocrine therapy resistance invariably develops in advanced estrogen receptor-positive (ER+) breast cancer, but the underlying mechanisms are largely unknown. We have identified C-terminal SRC kinase (CSK) as a critical node in a previously unappreciated negative feedback loop that limits the efficacy of current ER-targeted therapies. Estrogen directly drives CSK expression in ER+ breast cancer. At low CSK levels, as is ... [more]
Proc. Natl. Acad. Sci. U.S.A. Dec. 31, 2017; 115(31);7869-7878 [Pubmed: 29987050]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507)
- phenotype: viability (PATO:0000169)
Additional Notes
- CRISPR GI screen
- Cell Line:T47D
- Experimental Setup: Timecourse, negative selection, viability
- GIST: A-phenotypic negative genetic interaction
- Library: Geckov2
- Significance Threshold: FDR<0.05
Curated By
- BioGRID