Rad27 and Exo1 function in different excision pathways for mismatch repair in Saccharomyces cerevisiae

Felipe A. Calil; Bin-Zhong Li; Kendall A. Torres; Katarina Nguyen; Nikki Bowen; Christopher D. Putnam; Richard D. Kolodner

doi:10.1038/s41467-021-25866-z

Nature Communications (Sep 2021)

Rad27 and Exo1 function in different excision pathways for mismatch repair in Saccharomyces cerevisiae

Felipe A. Calil,
Bin-Zhong Li,
Kendall A. Torres,
Katarina Nguyen,
Nikki Bowen,
Christopher D. Putnam,
Richard D. Kolodner

Affiliations

Felipe A. Calil: Ludwig Institute for Cancer Research, University of California School of Medicine
Bin-Zhong Li: Ludwig Institute for Cancer Research, University of California School of Medicine
Kendall A. Torres: Ludwig Institute for Cancer Research, University of California School of Medicine
Katarina Nguyen: Ludwig Institute for Cancer Research, University of California School of Medicine
Nikki Bowen: Ludwig Institute for Cancer Research, University of California School of Medicine
Christopher D. Putnam: Ludwig Institute for Cancer Research, University of California School of Medicine
Richard D. Kolodner: Ludwig Institute for Cancer Research, University of California School of Medicine

DOI: https://doi.org/10.1038/s41467-021-25866-z
Journal volume & issue: Vol. 12, no. 1
pp. 1 – 10

Abstract

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Defects in DNA mismatch repair (MMR) have been linked to inherited and sporadic cancers. Here the authors demonstrate that the DNA repair protein Rad27 (human FEN1) functions in one of three redundant mispair excision pathways, where its flap endonuclease activity catalyzes mispair excision.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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