BAIT
SLFN11
SLFN8/9
schlafen family member 11
GO Process (2)
GO Function (1)
GO Component (4)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Homo sapiens
PREY
DNAJA1
DJ-2, DjA1, HDJ2, HSDJ, HSJ2, HSPF4, NEDD7, hDJ-2, RP11-54K16.1
DnaJ (Hsp40) homolog, subfamily A, member 1
GO Process (9)
GO Function (7)
GO Component (5)
Gene Ontology Biological Process
- negative regulation of JUN kinase activity [IMP]
- negative regulation of apoptotic process [IMP]
- negative regulation of protein ubiquitination [IDA]
- positive regulation of apoptotic process [IMP]
- protein folding [TAS]
- protein localization to mitochondrion [IMP]
- protein refolding [IBA]
- regulation of protein transport [IDA]
- response to unfolded protein [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Affinity Capture-MS
An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner is identified by mass spectrometric methods.
Publication
SLFN11 promotes CDT1 degradation by CUL4 in response to replicative DNA damage, while its absence leads to synthetic lethality with ATR/CHK1 inhibitors.
Schlafen-11 (SLFN11) inactivation in ?50% of cancer cells confers broad chemoresistance. To identify therapeutic targets and underlying molecular mechanisms for overcoming chemoresistance, we performed an unbiased genome-wide RNAi screen in SLFN11-WT and -knockout (KO) cells. We found that inactivation of Ataxia Telangiectasia- and Rad3-related (ATR), CHK1, BRCA2, and RPA1 overcome chemoresistance to camptothecin (CPT) in SLFN11-KO cells. Accordingly, we validate ... [more]
Proc Natl Acad Sci U S A Dec. 09, 2020; 118(6); [Pubmed: 33536335]
Throughput
- Low Throughput
Curated By
- BioGRID