BAIT
ATR
FCTCS, FRP1, MEC1, SCKL, SCKL1
ATR serine/threonine kinase
GO Process (14)
GO Function (6)
GO Component (4)
Gene Ontology Biological Process
- DNA damage checkpoint [IDA]
- DNA repair [TAS]
- DNA replication [TAS]
- cell cycle [TAS]
- cellular response to DNA damage stimulus [TAS]
- cellular response to UV [IMP]
- cellular response to gamma radiation [IDA]
- double-strand break repair via homologous recombination [IBA]
- multicellular organismal development [TAS]
- negative regulation of DNA replication [IMP]
- peptidyl-serine phosphorylation [IDA]
- positive regulation of DNA damage response, signal transduction by p53 class mediator [IMP]
- protein autophosphorylation [IDA]
- replicative senescence [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
POLD1
CDC2, CRCS10, MDPL, POLD
polymerase (DNA directed), delta 1, catalytic subunit
GO Process (20)
GO Function (5)
GO Component (7)
Gene Ontology Biological Process
- DNA repair [TAS]
- DNA replication [IMP]
- DNA replication proofreading [IBA]
- DNA replication, removal of RNA primer [IBA]
- DNA strand elongation involved in DNA replication [TAS]
- DNA synthesis involved in DNA repair [IDA, IMP]
- base-excision repair [TAS]
- base-excision repair, gap-filling [IDA]
- fatty acid homeostasis [IMP]
- mitotic cell cycle [TAS]
- nucleotide-excision repair [TAS]
- nucleotide-excision repair, DNA gap filling [IC, IMP, TAS]
- regulation of mitotic cell cycle [IBA]
- response to UV [TAS]
- small molecule metabolic process [TAS]
- telomere maintenance [TAS]
- telomere maintenance via recombination [TAS]
- telomere maintenance via semi-conservative replication [TAS]
- transcription-coupled nucleotide-excision repair [TAS]
- translesion synthesis [IBA]
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
A synthetic lethal screen identifies ATR-inhibition as a novel therapeutic approach for POLD1-deficient cancers.
The phosphoinositide 3-kinase-related kinase ATR represents a central checkpoint regulator and mediator of DNA-repair. Its inhibition selectively eliminates certain subsets of cancer cells in various tumor types, but the underlying genetic determinants remain enigmatic. Here, we applied a synthetic lethal screen directed against 288 DNA-repair genes using the well-defined ATR knock-in model of DLD1 colorectal cancer cells to identify potential ... [more]
Oncotarget Feb. 09, 2016; 7(6);7080-95 [Pubmed: 26755646]
Throughput
- Low Throughput
Related interactions
Curated By
- BioGRID