ArticleProceedings of the National Academy of Sciences of the United States of America2026
Mechanism of MutLβ-dependent DNA expansions.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
Abstract
MutS and MutL proteins and their eukaryotic homologs have important functions in DNA metabolism. MutLβ (MLH1-PMS1 heterodimer) is a poorly understood eukaryotic MutL complex. Recent genetic studies have implicated MutLβ in the process of expansion of the short, tandem DNA repeat tracts that is responsible for the repeat expansion diseases. The function of MutLβ and the mechanism of MutLβ-dependent DNA expansions have not been established. We show here that MutLβ promotes MutSβ- and MutLγ-dependent DNA expansions in human cell extracts and defined systems. Importantly, DNA expansions that occur in human cell extracts in the presence of MutSβ and a low concentration of MutLγ require MutLβ. A MutSβ variant lacking the PCNA-binding motif is proficient in supporting MutLβ-promoted and MutLγ-dependent DNA expansions. We also show that MutLβ enhances the MutSβ-dependent endonuclease activity of MutLγ that incises the loop-lacking strand of loop-containing DNAs. MutLβ also increases the endonuclease activity of MutLγ in the presence of ATP-Mn
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