BAIT

DPB11

protein kinase activating protein DPB11, L000003001, YJL090C
DNA replication initiation protein; loads DNA pol epsilon onto pre-replication complexes at origins; checkpoint sensor recruited to stalled replication forks by the checkpoint clamp complex where it activates Mec1p; along with Rfa1p, binds to ultrafine anaphase bridges in mitotic cells and prevents accumulation of chromatin bridges by stimulating the Mec1p kinase and suppressing homologous recombination; ortholog of human TopBP1; forms nuclear foci upon DNA replication stress
Saccharomyces cerevisiae (S288c)
PREY

RFA1

BUF2, FUN3, RPA1, RPA70, replication factor A subunit protein RFA1, L000000204, L000001620, YAR007C
Subunit of heterotrimeric Replication Protein A (RPA); RPA is a highly conserved single-stranded DNA binding protein involved in DNA replication, repair, and recombination; RPA protects against inappropriate telomere recombination, and upon telomere uncapping, prevents cell proliferation by a checkpoint-independent pathway; role in DNA catenation/decatenation pathway of chromosome disentangling; relocalizes to the cytosol in response to hypoxia
Saccharomyces cerevisiae (S288c)

Reconstituted Complex

An interaction is detected between purified proteins in vitro.

Publication

Dpb11 may function with RPA and DNA to initiate DNA replication.

Bruck I, Dhingra N, Martinez MP, Kaplan DL

Dpb11 is required for the initiation of DNA replication in budding yeast. We found that Dpb11 binds tightly to single-stranded DNA (ssDNA) or branched DNA structures, while its human homolog, TopBP1, binds tightly to branched-DNA structures. We also found that Dpb11 binds stably to CDK-phosphorylated RPA, the eukaryotic ssDNA binding protein, in the presence of branched DNA. A Dpb11 mutant ... [more]

PLoS ONE May. 04, 2017; 12(5);e0177147 [Pubmed: 28467467]

Throughput

  • Low Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
DPB11 RFA1
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-0.3587BioGRID
1939186

Curated By

  • BioGRID