BAIT

CDC73

L000002792, YLR418C
Component of the Paf1p complex; binds to and modulates the activity of RNA polymerases I and II; required for expression of certain genes, modification of some histones, and telomere maintenance; involved in transcription elongation as demonstrated by the G-less-based run-on (GLRO) assay; protein abundance increases in response to DNA replication stress; human homologue, parafibromin, is a tumour suppressor linked to breast, renal and gastric cancers
Saccharomyces cerevisiae (S288c)
PREY

EFB1

TEF5, translation elongation factor 1 subunit beta, EF-1beta, eEF1Balpha, L000000542, YAL003W
Translation elongation factor 1 beta; stimulates nucleotide exchange to regenerate EF-1 alpha-GTP for the next elongation cycle; part of the EF-1 complex, which facilitates binding of aminoacyl-tRNA to the ribosomal A site
Saccharomyces cerevisiae (S288c)

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

Saccharomyces cerevisiae Genetics Predicts Candidate Therapeutic Genetic Interactions at the Mammalian Replication Fork.

van Pel DM, Stirling PC, Minaker SW, Sipahimalani P, Hieter P

The concept of synthetic lethality has gained popularity as a rational guide for predicting chemotherapeutic targets based on negative genetic interactions between tumor-specific somatic mutations and a second-site target gene. One hallmark of most cancers that can be exploited by chemotherapies is chromosome instability (CIN). Because chromosome replication, maintenance, and segregation represent conserved and cell-essential processes, they can be modeled ... [more]

G3 (Bethesda) Feb. 01, 2013; 3(2);273-82 [Pubmed: 23390603]

Quantitative Score

  • 0.000323485 [SGA Score]

Throughput

  • High Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • SGA analysis for synthetic lethal interactions between mutations whose human orthologs are found to be mutated in cancers, and the deletion mutant collection, where the interaction probability P < 0.05

Curated By

  • BioGRID