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
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
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.

Srivas R, Shen JP, Yang CC, Sun SM, Li J, Gross AM, Jensen J, Licon K, Bojorquez-Gomez A, Klepper K, Huang J, Pekin D, Xu JL, Yeerna H, Sivaganesh V, Kollenstart L, van Attikum H, Aza-Blanc P, Sobol RW, Ideker T

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