HDAC4 Degradation Mediates HDAC Inhibition-Induced Protective Effects Against Hypoxia/Reoxygenation Injury

Author:

Du Jianfeng1,Zhang Ling2,Zhuang Shougang3,Qin Gang Jian4,Zhao Ting cun1

Affiliation:

1. Department of Surgery; Boston University Medical School; Boston University; Roger Williams Medical Center; Providence Rhode Island

2. Department of Emergency Medicine; Rhode Island Hospital; Brown Medical School; Brown University; Providence Rhode Island

3. Department of Medicine; Rhode Island Hospital; Brown Medical School; Brown University; Providence Rhode Island

4. Feinberg Cardiovascular Research Institute; Northwestern University Feinberg School of Medicine; Chicago Illinois

Publisher

Wiley

Subject

Cell Biology,Clinical Biochemistry,Physiology

Reference32 articles.

1. Dose-dependent blockade to cardiomyocyte hypertrophy by histone deacetylase inhibitors;Antos;J Biol Chem,2003

2. The histone deacetylase inhibitor SAHA arrests cancer cell growth, up-regulates thioredoxin-binding protein-2, and down-regulates thioredoxin;Butler;Proc Natl Acad Sci U S A,2002

3. Ubiquitin-dependent degradation of HDAC4, a new regulator of random cell motility;Cernotta;Mol Biol Cell,2011

4. HDAC inhibition promotes cardiogenesis and the survival of embryonic stem cells through proteasome-dependent pathway;Chen;J Biol Chem,2011

5. A New Family of Human Histone Deacetylases Related to Saccharomyces cerevisiae HDA1p;Fischle;J Biol Chem,1999

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