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Abstract
Werner syndrome (WS) is an autosomal recessive disease caused by loss of function of WRN. WS is a segmental progeroid disease and shows early onset or increased frequency of many characteristics of normal aging. WRN possesses helicase, annealing, strand exchange, and exonuclease activities and acts on a variety of DNA substrates, even complex replication and re- combination intermediates. Here, we review the genetics, biochemistry, and probably physiological functions of the WRN protein. Although its precise role is unclear, evidence suggests WRN plays a role in pathways that respond to replication stress and maintain genome stability particularly in telomeric regions.
Document Type
Article
Publication Date
7-2024
Digital Object Identifier (DOI)
https://doi.org/10.3390/ijms25158300
Funding Information
This research received no external funding.
Repository Citation
Orren, David K. and Machwe, Amrita, "Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein" (2024). Markey Cancer Center Faculty Publications. 230.
https://uknowledge.uky.edu/markey_facpub/230
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Notes/Citation Information
© 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).