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

SCH9

HRM2, KOM1, serine/threonine protein kinase SCH9, L000001810, YHR205W
AGC family protein kinase; functional ortholog of mammalian S6 kinase; phosphorylated by Tor1p and required for TORC1-mediated regulation of ribosome biogenesis, translation initiation, and entry into G0 phase; involved in transactivation of osmostress-responsive genes; regulates G1 progression, cAPK activity and nitrogen activation of the FGM pathway; integrates nutrient signals and stress signals from sphingolipids to regulate lifespan
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

  • -3.04 [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).

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SCH9 SIC1
Negative Genetic
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.

High-0.1406BioGRID
2130255

Curated By

  • BioGRID