Lysine acetylation induced by chronic ethanol consumption impairs dynamin-mediated clathrin-coated vesicle release.

ABSTRACT:

Unlabelled

The liver is the major site of ethanol metabolism and thus sustains the most injury from chronic alcohol consumption. Ethanol metabolism by the hepatocyte leads to the generation of reactive metabolites and oxygen radicals that can readily adduct DNA, lipids, and proteins. More recently, it has become apparent that ethanol consumption also leads to increased post-translational modifications of the natural repertoire, including lysine hyperacetylation. Previously, we determined that alcohol consumption selectively impairs clathrin-mediated internalization in polarized hepatocytes. However, neither the step at which the block occurs nor the mechanism responsible for the defect have been identified. To identify the specific step at which clathrin-mediated internalization is

SUBMITTER: Shepard BD 

PROVIDER: S-EPMC3292665 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature