CHEK1
Gene Ontology Biological Process
- DNA damage checkpoint [IDA, IMP]
- DNA damage induced protein phosphorylation [IDA]
- DNA repair [IMP]
- DNA replication [TAS]
- G2 DNA damage checkpoint [IMP]
- cellular response to DNA damage stimulus [IMP]
- cellular response to mechanical stimulus [IEP]
- chromatin-mediated maintenance of transcription [ISS]
- negative regulation of mitosis [IDA]
- peptidyl-threonine phosphorylation [IDA]
- regulation of double-strand break repair via homologous recombination [IDA]
- regulation of histone H3-K9 acetylation [ISS]
- regulation of mitotic centrosome separation [IDA]
- regulation of transcription from RNA polymerase II promoter in response to UV-induced DNA damage [ISS]
- replicative senescence [NAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
TP53BP1
Gene Ontology Biological Process
- DNA repair [TAS]
- cellular response to DNA damage stimulus [IDA]
- double-strand break repair [TAS]
- double-strand break repair via homologous recombination [TAS]
- positive regulation of sequence-specific DNA binding transcription factor activity [IC]
- positive regulation of transcription from RNA polymerase II promoter [IMP]
- positive regulation of transcription, DNA-templated [NAS]
- transcription from RNA polymerase II promoter [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Biochemical Activity (Phosphorylation)
An interaction is inferred from the biochemical effect of one protein upon another, for example, GTP-GDP exchange activity or phosphorylation of a substrate by a kinase. The bait protein executes the activity on the substrate hit protein. A Modification value is recorded for interactions of this type with the possible values Phosphorylation, Ubiquitination, Sumoylation, Dephosphorylation, Methylation, Prenylation, Acetylation, Deubiquitination, Proteolytic Processing, Glucosylation, Nedd(Rub1)ylation, Deacetylation, No Modification, Demethylation.
Publication
Phosphorylation-dependent interactions of BLM and 53BP1 are required for their anti-recombinogenic roles during homologous recombination.
Mutations in bloom helicase protein (BLM) helicase cause Bloom syndrome, characterized by predisposition to almost all forms of cancer. We have demonstrated previously that endogenous BLM, signal transducer 53BP1 and RAD51 are present in a complex during replication stress. Using full-length recombinant proteins, we now provide evidence that these proteins physically interact. BLM interacts with checkpoint kinase (Chk) 1 via ... [more]
Throughput
- Low Throughput
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| TP53BP1 CHEK1 | Co-localization Co-localization Interaction inferred from two proteins that co-localize in the cell by indirect immunofluorescence only when in addition, if one gene is deleted, the other protein becomes mis-localized. Also includes co-dependent association of proteins with promoter DNA in chromatin immunoprecipitation experiments. | Low | - | BioGRID | 244995 |
Curated By
- BioGRID