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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/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#_4 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#_3 http://www.w3.org/ns/prov#value During fasting and many systemic diseases, muscle undergoes rapid loss of protein and functional capacity. To define the transcriptional changes triggering muscle atrophy and energy conservation in fasting, we used cDNA microarrays to compare mRNAs from muscles of control and food-deprived mice. Expression of 94% of genes did not change, but interesting patterns emerged among genes that were differentially expressed: 1) mRNAs encoding polyubiquitin, ubiquitin extension proteins, and many (but not all) proteasome subunits increased, which presumably contributes to accelerated protein breakdown; 2) a dramatic increase in mRNA for the ubiquitin ligase, atrogin-1, but not most E3s; 3) a significant suppression of mRNA for myosin binding protein H (but not other myofibrillar proteins) and IGF binding protein 5, which may favor cell protein loss; 4) decreases in mRNAs for several glycolytic enzymes and phosphorylase kinase subunits, and dramatic increases in mRNAs for pyruvate dehydrogenase kinase 4 and glutamine synthase, which should promote glucose sparing and gluconeogenesis. During fasting, metallothionein mRNA increased dramatically, mRNAs for extracellular matrix components fell, and mRNAs that may favor cap-independent mRNA translation rose. Significant changes occurred in mRNAs for many growth-related proteins and transcriptional regulators. These transcriptional changes indicate a complex adaptive program that should favor protein degradation and suppress glucose oxidation in muscle. Similar analysis of muscles atrophying for other causes is allowing us to identify a set of atrophy-specific changes in gene expression. http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#_3 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/12409312 http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#_4 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/12409312 http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#_3 http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU#pubinfo http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU http://purl.org/dc/terms/created 2014-07-03T14:30:06.867+02:00 http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RAU6QHCK9wkEsuX4FIFWrU5BbyvB8NSl_wyPQiaXgpVxU http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234