RAD5
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
CDC28
Gene Ontology Biological Process
- 7-methylguanosine mRNA capping [IMP]
- chromatin remodeling [IMP]
- meiotic DNA double-strand break processing [IGI]
- negative regulation of double-strand break repair via nonhomologous end joining [IMP]
- negative regulation of meiotic cell cycle [IMP]
- negative regulation of mitotic cell cycle [IDA]
- negative regulation of sister chromatid cohesion [IMP]
- negative regulation of transcription, DNA-templated [IDA, IMP]
- peptidyl-serine phosphorylation [IDA]
- phosphorylation of RNA polymerase II C-terminal domain [IDA]
- positive regulation of meiotic cell cycle [IDA, IMP]
- positive regulation of mitotic cell cycle [IMP]
- positive regulation of nuclear cell cycle DNA replication [IDA, IMP]
- positive regulation of spindle pole body separation [IGI, IMP]
- positive regulation of transcription from RNA polymerase II promoter [IMP]
- positive regulation of transcription, DNA-templated [IDA, IGI]
- positive regulation of triglyceride catabolic process [IGI, IMP]
- protein phosphorylation [IDA]
- regulation of budding cell apical bud growth [IGI, IMP]
- regulation of double-strand break repair via homologous recombination [IMP]
- regulation of filamentous growth [IMP]
- regulation of protein localization [IMP]
- synaptonemal complex assembly [IMP]
- vesicle-mediated transport [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Dosage Lethality
A genetic interaction is inferred when over expression or increased dosage of one gene causes lethality in a strain that is mutated or deleted for another gene.
Publication
Rad5 dysregulation drives hyperactive recombination at replication forks resulting in cisplatin sensitivity and genome instability.
The postreplication repair gene, HLTF, is often amplified and overexpressed in cancer. Here we model HLTF dysregulation through the functionally conserved Saccharomyces cerevisiae ortholog, RAD5. Genetic interaction profiling and landscape enrichment analysis of RAD5 overexpression (RAD5OE) reveals requirements for genes involved in recombination, crossover resolution, and DNA replication. While RAD5OE and rad5Δ both cause cisplatin sensitivity and share many genetic ... [more]
Throughput
- High Throughput
Ontology Terms
- phenotype: inviable (APO:0000112)
Additional Notes
- over-expression of Rad5 is lethal in combination with a temperature sensitive mutant of the hit gene
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| CDC28 RAD5 | Dosage Lethality Dosage Lethality A genetic interaction is inferred when over expression or increased dosage of one gene causes lethality in a strain that is mutated or deleted for another gene. | Low | - | BioGRID | 2452230 | |
| CDC28 RAD5 | Phenotypic Enhancement 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. | Low | - | BioGRID | 353053 | |
| CDC28 RAD5 | Synthetic Growth Defect Synthetic Growth Defect A genetic interaction is inferred when mutations in separate genes, each of which alone causes a minimal phenotype, result in a significant growth defect under a given condition when combined in the same cell. | Low | - | BioGRID | 662629 |
Curated By
- BioGRID