| pubmed-article:17469125 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17469125 | lifeskim:mentions | umls-concept:C0004391 | lld:lifeskim |
| pubmed-article:17469125 | lifeskim:mentions | umls-concept:C0751713 | lld:lifeskim |
| pubmed-article:17469125 | lifeskim:mentions | umls-concept:C1710236 | lld:lifeskim |
| pubmed-article:17469125 | lifeskim:mentions | umls-concept:C2353566 | lld:lifeskim |
| pubmed-article:17469125 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:17469125 | pubmed:dateCreated | 2007-5-3 | lld:pubmed |
| pubmed-article:17469125 | pubmed:abstractText | Sporadic Inclusion Body Myositis (sIBM) is the most common acquired muscle disease in patients above 50 years of age. Apart from inflammation in the skeletal muscle, overexpression of amyloid precursor protein (APP) and intracellular accumulation of its proteolytic fragment beta-amyloid play a central role in the pathogenesis of sIBM. In neurodegenerative disorders, similar aggregations of aberrant proteins have recently been shown to be susceptible to autophagic degradation. Therefore, we analyzed macroautophagy of APP in human muscle cell lines and sIBM muscle biopsies. | lld:pubmed |
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| pubmed-article:17469125 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17469125 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17469125 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17469125 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17469125 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17469125 | pubmed:month | May | lld:pubmed |
| pubmed-article:17469125 | pubmed:issn | 0364-5134 | lld:pubmed |
| pubmed-article:17469125 | pubmed:author | pubmed-author:MünzChristian... | lld:pubmed |
| pubmed-article:17469125 | pubmed:author | pubmed-author:DalakasMarino... | lld:pubmed |
| pubmed-article:17469125 | pubmed:author | pubmed-author:LünemannJan... | lld:pubmed |
| pubmed-article:17469125 | pubmed:author | pubmed-author:SchmidtJensJ | lld:pubmed |
| pubmed-article:17469125 | pubmed:author | pubmed-author:SchmidDorothe... | lld:pubmed |
| pubmed-article:17469125 | pubmed:author | pubmed-author:WredeArneA | lld:pubmed |
| pubmed-article:17469125 | pubmed:author | pubmed-author:BarthelKonsta... | lld:pubmed |
| pubmed-article:17469125 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17469125 | pubmed:volume | 61 | lld:pubmed |
| pubmed-article:17469125 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17469125 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17469125 | pubmed:pagination | 476-83 | lld:pubmed |
| pubmed-article:17469125 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:17469125 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17469125 | pubmed:articleTitle | Beta-amyloid is a substrate of autophagy in sporadic inclusion body myositis. | lld:pubmed |
| pubmed-article:17469125 | pubmed:affiliation | Laboratory of Viral Immunobiology, Christopher H. Browne Center for Immunology and Immune Diseases, The Rockefeller University, New York, NY 10021, USA. | lld:pubmed |
| pubmed-article:17469125 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17469125 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17469125 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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