BAIT

SST2

GTPase-activating protein SST2, L000002093, YLR452C
GTPase-activating protein for Gpa1p; regulates desensitization to alpha factor pheromone; also required to prevent receptor-independent signaling of the mating pathway; member of the RGS (regulator of G-protein signaling) family
GO Process (2)
GO Function (1)
GO Component (1)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

IKS1

protein kinase IKS1, L000004209, YJL057C
Protein kinase of unknown cellular role; putative serine/threonine kinase; expression is induced during mild heat stress; deletion mutants are hypersensitive to copper sulphate and resistant to sorbate; interacts with an N-terminal fragment of Sst2p
Kinome Project (Sc)
GO Process (1)
GO Function (1)
GO Component (0)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Saccharomyces cerevisiae (S288c)

Two-hybrid

Bait protein expressed as a DNA binding domain (DBD) fusion and prey expressed as a transcriptional activation domain (TAD) fusion and interaction measured by reporter gene activation.

Publication

Regulation of stress response signaling by the N-terminal dishevelled/EGL-10/pleckstrin domain of Sst2, a regulator of G protein signaling in Saccharomyces cerevisiae.

Burchett SA, Flanary P, Aston C, Jiang L, Young KH, Uetz P, Fields S, Dohlman HG

All members of the regulator of G protein signaling (RGS) family contain a conserved core domain that can accelerate G protein GTPase activity. The RGS in yeast, Sst2, can inhibit a G protein signal leading to mating. In addition, some RGS proteins contain an N-terminal domain of unknown function. Here we use complementary whole genome analysis methods to investigate the ... [more]

J. Biol. Chem. Jun. 21, 2002; 277(25);22156-67 [Pubmed: 11940600]

Throughput

  • Low Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
IKS1 SST2
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-0.186BioGRID
2135196

Curated By

  • BioGRID