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ATP depletion increases phosphorylation of elongation factor eEF2 in adult cardiomyocytes independently of inhibition of mTOR signalling
Author(s) -
McLeod Laura E,
Proud Christopher G
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03582-2
Subject(s) - phosphorylation , elongation factor , microbiology and biotechnology , kinase , pi3k/akt/mtor pathway , protein phosphorylation , protein biosynthesis , elongation , protein kinase a , translation (biology) , phosphorylation cascade , biology , biochemistry , chemistry , signal transduction , rna , ribosome , messenger rna , gene , materials science , ultimate tensile strength , metallurgy
Translation elongation consumes a high proportion of cellular energy and can be regulated by phosphorylation of elongation factor eEF2 which inhibits its activity. We have studied the effects of ATP depletion on the phosphorylation of eEF2 in adult rat ventricular cardiomyocytes. Energy depletion rapidly leads to inhibition of protein synthesis and increased phosphorylation of eEF2. Stimulation of the AMP‐activated protein kinase also causes increases eEF2 phosphorylation. Only at later times is an effect on mTOR signalling observed. These data suggest that energy depletion leads to inhibition of protein synthesis through phosphorylation of eEF2 independently of inhibition of mTOR signalling.