Chromatin to Clinic: The Molecular Rationale for PARP1 Inhibitor Function.

Authors

Felix Y. Feng, University Of MichiganFollow
Johann S. de Bono, The Royal Marsden NHS Foundation TrustFollow
Mark A. Rubin, Weill Cornell Medical CollegeFollow
Karen E Knudsen, Thomas Jefferson UniversityFollow

Document Type

Article

Publication Date

6-18-2015

Comments

This article has been peer reviewed. It is the authors' final version prior to publication in Molecular Cell

Volume 58, Issue 6, June 2015, Pages 925-934.

The published version is available at DOI: 10.1016/j.molcel.2015.04.016. Copyright © Cell Press

Abstract

Poly(ADP-ribose) polymerase 1 (PARP1) inhibitors were recently shown to have potential clinical impact in a number of disease settings, particularly as related to cancer therapy, treatment for cardiovascular dysfunction, and suppression of inflammation. The molecular basis for PARP1 inhibitor function is complex, and appears to depend on the dual roles of PARP1 in DNA damage repair and transcriptional regulation. Here, the mechanisms by which PARP-1 inhibitors elicit clinical response are discussed, and strategies for translating the preclinical elucidation of PARP-1 function into advances in disease management are reviewed.

Recommended Citation

Feng, Felix Y.; de Bono, Johann S.; Rubin, Mark A.; and Knudsen, Karen E, "Chromatin to Clinic: The Molecular Rationale for PARP1 Inhibitor Function." (2015). Department of Cancer Biology Faculty Papers. Paper 90.
https://jdc.jefferson.edu/cbfp/90

PubMed ID

26091341