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TRAF2 expression in differentiated muscle
Author(s) -
MacLachlan Timothy K.,
Giordano Antonio
Publication year - 1998
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19981215)71:4<461::aid-jcb1>3.0.co;2-0
Subject(s) - myogenesis , traf2 , skeletal muscle , myocyte , tumor necrosis factor alpha , microbiology and biotechnology , biology , in vitro , medicine , endocrinology , biochemistry , tumor necrosis factor receptor
Recent data involving traf2 knockout mice have suggested a necessity of the protein in viability of skeletal muscle tissue. traf2 −/− mice are born with decreased muscle mass that is hypothesized to be due to the increased circulating tumor necrosis factor in these mice. We show that TRAF2 protein is present at high levels in terminally differentiated skeletal muscle in the developing mouse. In vitro differentiation of mouse myoblasts displays a dramatic increase in TRAF2 protein levels. Although basal NF‐κB activity decreases during myogenesis, TNF‐induced NF‐κB activity is 10 times greater in myotubes compared with myoblasts, presumably because of the stockpiling of TRAF2 protein in these cells. This may represent a strong anti‐apoptotic TRAF2‐mediated response specifically tailored to myotubes. These data help explain why muscle integrity is at risk in traf2 −/− mice. J. Cell. Biochem. 71:461–466, 1998. © 1998 Wiley‐Liss, Inc.