NDLI: How do drug-induced topoisomerase I-DNA lesions signal to the molecular interaction network that regulates cell cycle checkpoints, DNA replication, and DNA repair?

Content Provider	Springer Nature Link
Author	Kohn, Kurt W. Shao, Rhong Guang Pommier, Yves
Copyright Year	2000
Abstract	Recent results suggest that potentially lethal DNA lesions may result when replication forks encounter trapped topoisomerase-DNA complexes or some other types of DNA damage. Such events produce what are called replication-encounter lesions. These lesions have the characteristic that they may allow single stranded DNA-associated replication protein A (RPA) to become juxtaposed to dsDNA end-associated DNA-protein kinase. Our results suggest that DNA-protein kinases may then hyperphosphorylate the RPA2 subunit. We discuss a possible pathway by which hyperphosphorylation of RPA2 could lead to the release of active p53. This could constitute a pathway for signaling the presence of replication-encounter lesions to the p53-dependent cell cycle arrest and/or apoptosis initiator systems. * DIRECT SUPPORT * A01Q2011 00008
Starting Page	175
Ending Page	180
Page Count	6
File Format	PDF
ISSN	10859195
Journal	Cell Biochemistry and Biophysics
Volume Number	33
Issue Number	2
e-ISSN	15590283
Language	English
Publisher	Humana Press
Publisher Date	2000-01-01
Publisher Place	Totowa
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Biochemistry Pharmacology/Toxicology Biotechnology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Biochemistry Biophysics

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How do drug-induced topoisomerase I-DNA lesions signal to the molecular interaction network that regulates cell cycle checkpoints, DNA replication, and DNA repair?