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Mouse heat shock transcription factor 1 deficiency alters cardiac redox homeostasis and increases mitochondrial oxidative damage

In this study, using heat shock factor 1 (Hsf1) knockout mice as a model, we tested the hypothesis that HSF1-dependent regulation of heat shock proteins (Hsps) is required to maintain redox state and attenuate oxidative damage in the normal heart. Here we report that, in mice, HSF1 deficiency reduce...

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Detalles Bibliográficos
Main Authors: Yan, Liang-Jun, Christians, Elisabeth S., Liu, Li, Xiao, XianZhong, Sohal, Rajindar S., Benjamin, Ivor J.
Formato: Artigo
Idioma:Inglês
Publicado: Oxford University Press 2002
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Acceso en liña:https://ncbi.nlm.nih.gov/pmc/articles/PMC129050/
https://ncbi.nlm.nih.gov/pubmed/12356732
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/emboj/cdf528
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