Role of the ubiquitin-proteasome pathway in sepsis-induced muscle catabolism.

Abstract:

:Several lines of evidence suggest that the ubiquitin-proteasome pathway is involved in sepsis-induced muscle catabolism. The gene expression of ubiquitin and several of the proteasome subunits was increased in muscle from both septic rats and patients. In other studies, the activity of isolated 20S proteasomes was stimulated in septic muscles. Sepsis-induced increase in muscle total and myofibrillar protein breakdown was inhibited with specific proteasome blockers. Although the ubiquitin-proteasome pathway is upregulated in septic muscle, it is still unclear how the myofibrillar proteins actin and myosin are ubiquitinated and become substrates for the 26S proteasome. Recent studies suggest that a calcium-dependent, calpain-mediated process releases myofilaments from the Z-disks during sepsis. It is possible that this process exposes destabilizing N-terminal residues on actin and myosin, making them suitable substrates for the N-end rule pathway involving the 14 kD ubiquitin-conjugating enzyme E214k and the ubiquitin-protein ligase E3alpha.

journal_name

Mol Biol Rep

authors

Hasselgren PO

doi

10.1023/a:1006916206260

keywords:

subject

Has Abstract

pub_date

1999-04-01 00:00:00

pages

71-6

issue

1-2

eissn

0301-4851

issn

1573-4978

journal_volume

26

pub_type

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