ArticleMolecular microbiology2012
Brh2 domain function distinguished by differential cellular responses to DNA damage and replication stress.
Article in Molecular microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- The insertion of a mitochondrial selfish element into the nuclear genome and its consequences.Ecology and evolution · 2020Article
- Collaboration in the actions of Brh2 with resolving functions during DNA repair and replication stress in Ustilago maydis.DNA repair · 2018Article
- Bioavailability of Nutritional Resources From Cells Killed by Oxidation Supports Expansion of Survivors inFrontiers in microbiology · 2018Article
- Dual DNA-binding domains shape the interaction of Brh2 with DNA.DNA repair · 2014Article
- CBX8, a novel DNA repair protein, promotes tumorigenesis in human esophageal carcinoma.International journal of clinical and experimental pathology · 2014Article
- Homologous recombination as a replication fork escort: fork-protection and recovery.Biomolecules · 2012Article
- Dss1 release activates DNA binding potential in Brh2.Biochemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutants of the fungus Ustilago maydis defective in the RecQ helicase Blm are highly sensitive to killing by the DNA replication stressor hydroxyurea. This sensitivity or toxicity is dependent on the homologous recombination (HR) system and apparently results from formation of dead-end HR DNA intermediates. HU toxicity can be suppressed by deletion of the gene encoding Brh2, the BRCA2 orthologue that serves to regulate HR by mediating Rad51 filament formation on single-stranded DNA. Brh2 harbours two different DNA-binding domains that contribute to HR function. DNA-binding activity from a single domain is sufficient to provide Brh2 functional activity in HR, but to enable HU-induced killing two functional DNA-binding domains must be present. Despite this stringent requirement for dual functioning domains, the source of DNA-binding domains is less critical in that heterologous domains can substitute for the native endogenous ones. The results suggest a model in which the nature of the DNA lesion is an important determinant in the functional response of Brh2 action.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.