ArticleCell cycle (Georgetown, Tex.)2013
Detection of an altered heterochromatin structure in the absence of the nucleotide excision repair protein Rad4 in Saccharomyces cerevisiae.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- XPC: Going where no DNA damage sensor has gone before.DNA repair · 2015Review
- A Synthetic Interaction between CDC20 and RAD4 in Saccharomyces cerevisiae upon UV Irradiation.Molecular biology international · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Rad4p is a DNA damage recognition protein essential for global genomic nucleotide excision repair in Saccharomyces cerevisiae. Here, we show that Rad4p binds to the heterochromatic HML locus. In a yeast mutant lacking Rad4p, an increased level of SIR complex binding at the HML locus is accompanied by an altered, more compact heterochromatin structure, as revealed by a topological analysis of chromatin circles released from the locus. In addition, gene silencing at the HML locus is enhanced in the rad4Δ mutant. Importantly, re-expression of Rad4p in the rad4Δ mutant restores the altered heterochromatin structure to a conformation similar to that detected in wild-type cells. These findings reveal a novel role of Rad4p in the regulation of heterochromatin structure and gene silencing.
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Registered trials
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