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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#_5 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#_4 http://www.w3.org/ns/prov#value Muscle wasting accompanies aging and pathological conditions ranging from cancer, cachexia, and diabetes to denervation and immobilization. We show that activation of NF-kappaB, through muscle-specific transgenic expression of activated IkappaB kinase beta (MIKK), causes profound muscle wasting that resembles clinical cachexia. In contrast, no overt phenotype was seen upon muscle-specific inhibition of NF-kappaB through expression of IkappaBalpha superrepressor (MISR). Muscle loss was due to accelerated protein breakdown through ubiquitin-dependent proteolysis. Expression of the E3 ligase MuRF1, a mediator of muscle atrophy, was increased in MIKK mice. Pharmacological or genetic inhibition of the IKKbeta/NF-kappaB/MuRF1 pathway reversed muscle atrophy. Denervation- and tumor-induced muscle loss were substantially reduced and survival rates improved by NF-kappaB inhibition in MISR mice, consistent with a critical role for NF-kappaB in the pathology of muscle wasting and establishing it as an important clinical target for the treatment of muscle atrophy. We show that activation of NF-kappaB, through muscle-specific transgenic expression of activated IkappaB kinase beta (MIKK)... Expression of the E3 ligase MuRF1, a mediator of muscle atrophy, was increased in MIKK mice. http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#_4 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/15479644 http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#_5 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/15479644 http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#_4 http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs#pubinfo http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs http://purl.org/dc/terms/created 2014-07-03T14:30:28.649+02:00 http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RAyiJu2teMUWNeE04lFpb5H1_CcuL9Viy3puxWE_tsHvs http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234