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Titel:

Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity.

Dokumenttyp:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Autor(en):
Trivedi, CM; Luo, Y; Yin, Z; Zhang, M; Zhu, W; Wang, T; Floss, T; Goettlicher, M; Noppinger, PR; Wurst, W; Ferrari, VA; Abrams, CS; Gruber, PJ; Epstein, JA
Abstract:
In the adult heart, a variety of stresses induce re-expression of a fetal gene program in association with myocyte hypertrophy and heart failure. Here we show that histone deacetylase-2 (Hdac2) regulates expression of many fetal cardiac isoforms. Hdac2 deficiency or chemical histone deacetylase (HDAC) inhibition prevented the re-expression of fetal genes and attenuated cardiac hypertrophy in hearts exposed to hypertrophic stimuli. Resistance to hypertrophy was associated with increased expressio...     »
Zeitschriftentitel:
Nat Med
Jahr:
2007
Band / Volume:
13
Heft / Issue:
3
Seitenangaben Beitrag:
324-31
Sprache:
eng
Volltext / DOI:
doi:10.1038/nm1552
PubMed:
http://view.ncbi.nlm.nih.gov/pubmed/17322895
Print-ISSN:
1078-8956
TUM Einrichtung:
Institut für Toxikologie und Umwelthygiene
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