JCI table of contents: Oct. 25, 2007(e cardiac hypertrophy in part because ou...),Health

Date:10/25/2007

e cardiac hypertrophy, in part because our understanding of the molecular mechanisms by which cardiac hypertrophy can be reversed is limited. But now, new research in mice by Cam Patterson and colleagues at the University of North Carolina, Chapel Hill, has identified a mechanism by which the protein atrogin-1 disrupts pathways that promote cardiac hypertrophy.

In the study, atrogin-1 was shown to antagonize Akt-mediated cardiac hypertrophy. Atrogin-1 was found not to inhibit the function of Akt directly but to work by enhancing the activity of proteins known as Forkhead proteins, which repress Akt-dependent cardiac hypertrophy. Further analysis revealed that, at the molecular level, atrogin-1 enhances the activity of Forkhead proteins by inducing their ubiquitylation a process whereby the function of a protein is modified by being tagged with a very small, protein known as ubiquitin at a specific amino acid, lysine 63.

TITLE: Atrogin-1 inhibits Akt-dependent cardiac hypertrophy in mice via ubiquitin-dependent coactivation of Forkhead proteins

AUTHOR CONTACT:
Cam Patterson
University of North Carolina, Chapel Hill, North Carolina, USA.
Phone: (919) 843-6477; Fax: (919) 843-4585; Email: cpatters@med.unc.edu.

Hui-Hua Li,
Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, Peoples Republic of China.
Phone and Fax: 86-10-6529-6494; E-mail: hhli1995@yahoo.com.

View the PDF of this article at: https://www.the-jci.org/article.php?id=31757

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AUTOIMMUNITY: Histamine receptor makes T cells attack

Mice lacking the histamine H1 receptor (H1R) are less susceptible than normal mice to both experimental autoimmune encephalomyelitis (EAE; a mouse model of multiple sclerosis) and experimental autoimmune orch
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Contact: Karen Honey press_releases@the-jci.org 215-573-1850 Journal of Clinical Investigation Source:Eurekalert

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