Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase
Author:
Affiliation:
1. Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, DK-2200 Copenhagen, Denmark
2. Laboratory of Molecular Gerontology, National Institute on Aging, 251 Bayview Blvd, Baltimore, MD, 21224, USA
Abstract
Funder
Nordea Foundation
EU Joint Programme – Neurodegenerative Disease Research
Innovation Fund Denmark
Olav Thon Foundation Norway
Novo Nordisk Foundation
National Institute on Aging
Company of Biologists
Publisher
Oxford University Press (OUP)
Subject
Genetics
Link
http://academic.oup.com/nar/article-pdf/48/12/6530/33468706/gkaa392.pdf
Reference96 articles.
1. Aging in Rothmund-Thomson syndrome and related RECQL4 genetic disorders;Lu;Ageing Res. Rev.,2017
2. RECQL4 in genomic instability and aging;Croteau;Trends Genet.,2012
3. Human premature aging, DNA repair and RecQ helicases;Brosh;Nucleic Acids Res.,2007
4. Human RecQ helicases in DNA repair, recombination, and replication;Croteau;Annu. Rev. Biochem.,2014
5. The mutation spectrum in RECQL4 diseases;Siitonen;Eur. J. Hum. Genet.,2009
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