The HINT1 tumor suppressor regulates both γ-H2AX and ATM in response to DNA damage
Author:
Affiliation:
1. Herbert Irving Comprehensive Cancer Center
2. Center for Radiological Research
3. Department of Environmental Health Science,
4. Department of Medicine, Columbia University, New York, NY 10032
Abstract
Publisher
Rockefeller University Press
Subject
Cell Biology
Link
http://rupress.org/jcb/article-pdf/183/2/253/1340069/jcb_200711150.pdf
Reference51 articles.
1. The neurodegenerative disease protein aprataxin resolves abortive DNA ligation intermediates
2. RGSZ1 interacts with protein kinase C interacting protein PKCI-1 and modulates mu opioid receptor signaling
3. DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
4. Replication protein A and γ-H2AX foci assembly is triggered by cellular response to DNA double-strand breaks
5. Atm selectively regulates distinct p53-dependent cell-cycle checkpoint and apoptotic pathways
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