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

SLD7

YOR29-11, YOR060C
Protein with a role in chromosomal DNA replication; interacts with Sld3p and reduces its affinity for Cdc45p; deletion mutant has aberrant mitochondria
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
SLD7 RAD53
Synthetic Lethality
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.

Low-BioGRID
856810

Curated By

  • BioGRID