FAM111A protects replication forks from protein obstacles via its trypsin-like domain

Yusuke Kojima; Yuka Machida; Sowmiya Palani; Thomas R. Caulfield; Evette S. Radisky; Scott H. Kaufmann; Yuichi J. Machida

doi:10.1038/s41467-020-15170-7

Nature Communications (Mar 2020)

FAM111A protects replication forks from protein obstacles via its trypsin-like domain

Yusuke Kojima,
Yuka Machida,
Sowmiya Palani,
Thomas R. Caulfield,
Evette S. Radisky,
Scott H. Kaufmann,
Yuichi J. Machida

Affiliations

Yusuke Kojima: Department of Oncology, Mayo Clinic
Yuka Machida: Department of Oncology, Mayo Clinic
Sowmiya Palani: Department of Biochemistry and Molecular Biology, Mayo Clinic
Thomas R. Caulfield: Department of Neuroscience, Mayo Clinic
Evette S. Radisky: Department of Cancer Biology, Mayo Clinic
Scott H. Kaufmann: Department of Oncology, Mayo Clinic
Yuichi J. Machida: Department of Oncology, Mayo Clinic

DOI: https://doi.org/10.1038/s41467-020-15170-7
Journal volume & issue: Vol. 11, no. 1
pp. 1 – 14

Abstract

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DNA-protein crosslinks represent obstacles on genomic DNA that can hamper progression of replication forks. Here, the authors reveal that FAM111A, a PCNA-interacting protein, plays part in mitigating the effect of protein obstacles on replication forks.

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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