Source:http://linkedlifedata.com/resource/pubmed/id/11919155
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2002-3-28
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pubmed:abstractText |
Although cytokine-induced nuclear factor kappaB (NF-kappaB) pathways are involved in muscle wasting subsequent to disease, their potential role in disuse muscle atrophy has not been characterized. Seven days of hind limb unloading led to a 10-fold activation of an NF-kappaB-dependent reporter in rat soleus muscle but not the atrophy-resistant extensor digitorum longus muscle. Nuclear levels of p50 were markedly up-regulated, c-Rel was moderately up-regulated, Rel B was down-regulated, and p52 and p65 were unchanged in unloaded solei. The nuclear IkappaB protein Bcl-3 was increased. There was increased binding to an NF-kappaB consensus oligonucleotide, and this complex bound antibodies to p50, c-Rel, and Bcl-3 but not other NF-kappaB family members. Tumor necrosis factor alpha (TNF-alpha) and TNF receptor-associated factor 2 protein were moderately down-regulated. There was no difference in p38, c-Jun NH(2)-terminal kinase or Akt activity, nor were activator protein 1 or nuclear factor of activated T cell-dependent reporters activated. Thus, whereas several NF-kappaB family members are up-regulated, the prototypical markers of cytokine-induced activation of NF-kappaB seen with disease-related wasting are not evident during disuse atrophy. Levels of an anti-apoptotic NF-kappaB target, Bcl-2, were increased fourfold whereas proapoptotic proteins Bax and Bak decreased. The evidence presented here suggests that disuse muscle atrophy is associated with activation of an alternative NF-kappaB pathway that involves the activation of p50 but not p65.
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pubmed:grant | |
pubmed:keyword | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B p50 Subunit,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/proto-oncogene protein bcl-3
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1530-6860
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
16
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
529-38
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11919155-Animals,
pubmed-meshheading:11919155-Cell Nucleus,
pubmed-meshheading:11919155-Consensus Sequence,
pubmed-meshheading:11919155-Electrophoretic Mobility Shift Assay,
pubmed-meshheading:11919155-Female,
pubmed-meshheading:11919155-Genes, Reporter,
pubmed-meshheading:11919155-Hindlimb Suspension,
pubmed-meshheading:11919155-I-kappa B Kinase,
pubmed-meshheading:11919155-Models, Biological,
pubmed-meshheading:11919155-Muscle, Skeletal,
pubmed-meshheading:11919155-Muscular Atrophy,
pubmed-meshheading:11919155-NF-kappa B,
pubmed-meshheading:11919155-NF-kappa B p50 Subunit,
pubmed-meshheading:11919155-Protein-Serine-Threonine Kinases,
pubmed-meshheading:11919155-Proto-Oncogene Proteins,
pubmed-meshheading:11919155-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:11919155-Rats,
pubmed-meshheading:11919155-Signal Transduction,
pubmed-meshheading:11919155-Transcription Factors,
pubmed-meshheading:11919155-Tumor Necrosis Factor-alpha
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pubmed:year |
2002
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pubmed:articleTitle |
Activation of an alternative NF-kappaB pathway in skeletal muscle during disuse atrophy.
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pubmed:affiliation |
Boston University, Department of Health Sciences, Boston, Massachusetts 02215, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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