These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Activation of AMP-activated protein kinase (AMPK) inhibits protein synthesis: a potential strategy to prevent the development of cardiac hypertrophy. Author: Chan AY, Dyck JR. Journal: Can J Physiol Pharmacol; 2005 Jan; 83(1):24-8. PubMed ID: 15759047. Abstract: A necessary mediator of cardiac myocyte enlargement is protein synthesis, which is controlled, in part, by the highly energy-consuming process of peptide-chain elongation. Recently, AMP-activated protein kinase (AMPK), which is a key regulator of cellular energy homeostasis, has been shown to phosphorylate a number of enzymes involved in the control of protein synthesis. Since AMPK may inhibit protein synthesis via a number of different pathways, it is possible that AMPK is also a key regulator of cardiac hypertrophy. Recent advances linking AMPK and the energy status of the cell to the regulation of protein synthesis and (or) cardiac myocyte hypertrophy will be discussed.[Abstract] [Full Text] [Related] [New Search]