BAIT

RAD53

LSD1, MEC2, SPK1, serine/threonine/tyrosine protein kinase RAD53, L000001573, YPL153C
DNA damage response protein kinase; required for cell-cycle arrest in response to DNA damage; activated by trans autophosphorylation when interacting with hyperphosphorylated Rad9p; also interacts with ARS1 and plays a role in initiation of DNA replication; activates the downstream kinase Dun1p; differentially senses mtDNA depletion and mitochondrial ROS; required for regulation of copper genes in response to DNA-damaging agents; relocalizes to cytosol in response to hyoxia
Kinome Project (Sc)
Saccharomyces cerevisiae (S288c)
PREY

TAF12

TAF61, TAF68, TafII61, TafII68, L000003462, YDR145W
Subunit (61/68 kDa) of TFIID and SAGA complexes; involved in RNA polymerase II transcription initiation and in chromatin modification, similar to histone H2A
Saccharomyces cerevisiae (S288c)

Proximity Label-MS

An interaction is inferred when a bait-enzyme fusion protein selectively modifies a vicinal protein with a diffusible reactive product, followed by affinity capture of the modified protein and identification by mass spectrometric methods.

Publication

Checkpoint kinase interaction with DNA polymerase alpha regulates replication progression during stress.

Hadjicharalambous A, Whale AJ, Can G, Skehel JM, Houseley JM, Zegerman P

Background: In eukaryotes, replication stress activates a checkpoint response, which facilitates genome duplication by stabilising the replisome. How the checkpoint kinases regulate the replisome remains poorly understood. The aim of this study is to identify new targets of checkpoint kinases within the replisome during replication stress. Methods: Here we use an unbiased biotin proximity-ligation approach in Saccharomyces cerevisiae to identify ... [more]

Wellcome Open Res Sep. 28, 2023; 8();327 [Pubmed: 37766847]

Throughput

  • High Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
RAD53 TAF12
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-0.2475BioGRID
1955391

Curated By

  • BioGRID