TRP53BP1
Gene Ontology Biological Process
Gene Ontology Molecular Function- RNA polymerase II activating transcription factor binding [ISO]
- RNA polymerase II transcription cofactor activity [ISO]
- damaged DNA binding [IDA]
- methylated histone binding [ISO]
- p53 binding [ISO]
- protein binding [IPI]
- sequence-specific DNA binding [IDA]
- telomeric DNA binding [IDA]
- transcription factor binding [TAS]
- RNA polymerase II activating transcription factor binding [ISO]
- RNA polymerase II transcription cofactor activity [ISO]
- damaged DNA binding [IDA]
- methylated histone binding [ISO]
- p53 binding [ISO]
- protein binding [IPI]
- sequence-specific DNA binding [IDA]
- telomeric DNA binding [IDA]
- transcription factor binding [TAS]
Gene Ontology Cellular Component
TERF1
Gene Ontology Biological Process
- age-dependent telomere shortening [ISO]
- mitotic spindle assembly checkpoint [ISO]
- negative regulation of DNA replication [ISO]
- negative regulation of telomerase activity [ISO]
- negative regulation of telomere maintenance via telomerase [ISO]
- positive regulation of apoptotic process [ISO]
- positive regulation of microtubule polymerization [ISO]
- positive regulation of mitosis [ISO]
- positive regulation of mitotic cell cycle [ISO]
- protein homooligomerization [ISO]
- telomere maintenance via telomerase [ISO]
- telomere maintenance via telomere shortening [IBA]
- telomeric loop formation [IBA]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Phenotypic Enhancement
A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.
Publication
53BP1 deficiency combined with telomere dysfunction activates ATR-dependent DNA damage response.
TRF1 protects mammalian telomeres from fusion and fragility. Depletion of TRF1 leads to telomere fusions as well as accumulation of γ-H2AX foci and activation of both the ataxia telangiectasia mutated (ATM)- and the ataxia telangiectasia and Rad3 related (ATR)-mediated deoxyribonucleic acid (DNA) damage response (DDR) pathways. 53BP1, which is also present at dysfunctional telomeres, is a target of ATM that ... [more]
Throughput
- Low Throughput
Additional Notes
- figure 1. MEFs doubly deficient for TRF1 and 53BP1 show decreased chromosome-type end to end fusions but increased telomere recombination.
- figure 2. 53BP1 deficiency in TRF1del/del-immortalized MEFs leads to stronger CHK1 activation
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| TRP53BP1 TERF1 | Phenotypic Suppression Phenotypic Suppression A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene. | Low | - | BioGRID | 668589 | |
| TRP53BP1 TERF1 | Phenotypic Suppression Phenotypic Suppression A genetic interaction is inferred when mutation or over expression of one gene results in suppression of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene. | Low | - | BioGRID | 668318 | |
| TRP53BP1 TERF1 | 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 | 668591 |
Curated By
- BioGRID