BAIT
REV3L
POLZ, REV3, RP5-1112D6.1
REV3-like, polymerase (DNA directed), zeta, catalytic subunit
GO Process (3)
GO Function (3)
GO Component (3)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
CACNA1A
APCA, BI, CACNL1A4, CAV2.1, EA2, FHM, HPCA, MHP, MHP1, SCA6
calcium channel, voltage-dependent, P/Q type, alpha 1A subunit
GO Process (9)
GO Function (4)
GO Component (5)
Gene Ontology Biological Process
- calcium ion import [IBA]
- cell death [IDA]
- energy reserve metabolic process [TAS]
- membrane depolarization [TAS]
- membrane depolarization during action potential [IBA]
- positive regulation of cytosolic calcium ion concentration [IDA, ISS]
- regulation of insulin secretion [TAS]
- small molecule metabolic process [TAS]
- synaptic transmission [IBA, TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Synthetic Growth Defect
A genetic interaction is inferred when mutations in separate genes, each of which alone causes a minimal phenotype, result in a significant growth defect under a given condition when combined in the same cell.
Publication
Whole genome RNAi screens reveal a critical role of REV3 in coping with replication stress.
REV3, the catalytic subunit of translesion polymerase zeta (polζ), is commonly associated with DNA damage bypass and repair. Despite sharing accessory subunits with replicative polymerase δ, very little is known about the role of polζ in DNA replication. We previously demonstrated that inhibition of REV3 expression induces persistent DNA damage and growth arrest in cancer cells. To reveal determinants of ... [more]
Mol Oncol Dec. 01, 2014; 8(8);1747-59 [Pubmed: 25113059]
Quantitative Score
- 0.002291383 [Confidence Score]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507)
Additional Notes
- RNAi screen for synthetic sickness/lethality in REV3-deficient cells
- Table 1 and Table 2
Curated By
- BioGRID