BAIT
SIC1
SDB25, cyclin-dependent protein serine/threonine kinase inhibiting protein SIC1, L000001886, L000001822, YLR079W
Cyclin-dependent kinase inhibitor (CKI); inhibitor of Cdc28-Clb kinase complexes that controls G1/S phase transition, preventing premature S phase and ensuring genomic integrity; phosphorylated by Clb5/6-Cdk1 and Cln1/2-Cdk1 kinase which regulate timing of Sic1p degradation; phosphorylation targets Sic1p for SCF(CDC4)-dependent turnover; functional homolog of mammalian Kip1
GO Process (3)
GO Function (1)
GO Component (2)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Saccharomyces cerevisiae (S288c)
PREY
PSY2
YNL201C
Subunit of protein phosphatase PP4 complex; Pph3p and Psy2p form the active complex, Psy4p may provide additional substrate specificity; regulates recovery from the DNA damage checkpoint, the gene conversion- and single-strand annealing-mediated pathways of meiotic double-strand break repair and efficient Non-Homologous End-Joining (NHEJ) pathway; Pph3p and Psy2p localize to foci on meiotic chromosomes; putative homolog of mammalian R3
GO Process (6)
GO Function (1)
GO Component (3)
Gene Ontology Biological Process
- cellular response to DNA damage stimulus [IGI]
- negative regulation of DNA damage checkpoint [IMP]
- negative regulation of glucose mediated signaling pathway [IMP]
- positive regulation of double-strand break repair via nonhomologous end joining [IMP]
- protein dephosphorylation [IMP]
- signal transduction involved in meiotic recombination checkpoint [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Saccharomyces cerevisiae (S288c)
Negative Genetic
Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.
Publication
A Network of Conserved Synthetic Lethal Interactions for Exploration of Precision Cancer Therapy.
An emerging therapeutic strategy for cancer is to induce selective lethality in a tumor by exploiting interactions between its driving mutations and specific drug targets. Here we use a multi-species approach to develop a resource of synthetic lethal interactions relevant to cancer therapy. First, we screen in yeast ∼169,000 potential interactions among orthologs of human tumor suppressor genes (TSG) and ... [more]
Mol. Cell Aug. 04, 2016; 63(3);514-25 [Pubmed: 27453043]
Quantitative Score
- -3.5 [Confidence Score]
Throughput
- High Throughput
Ontology Terms
- phenotype: colony size (APO:0000063)
Additional Notes
- Untreated conditions. SGA was used to score genetic interactions based on the colony size of double versus single mutants. Genetic interactions were considered significant if they had an S score >= 2.0 for positive interactions (epistatic or suppressor interactions) and S score <= -2.5 for negative interactions (synthetic sick/lethal interactions).
Curated By
- BioGRID