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
SLC25A13
ARALAR2, CITRIN, CTLN2
solute carrier family 25 (aspartate/glutamate carrier), member 13
GO Process (13)
GO Function (4)
GO Component (3)
Gene Ontology Biological Process
- ATP biosynthetic process [IDA]
- L-aspartate transmembrane transport [IDA]
- L-glutamate transmembrane transport [IDA]
- L-glutamate transport [IDA]
- aspartate transport [IDA]
- carbohydrate metabolic process [TAS]
- cellular respiration [IDA]
- gluconeogenesis [TAS]
- glucose metabolic process [TAS]
- malate-aspartate shuttle [IDA]
- response to calcium ion [IDA]
- small molecule metabolic process [TAS]
- transport [NAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
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