pubmed-article:12200414 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C0007776 | lld:lifeskim |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C0022655 | lld:lifeskim |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C0001613 | lld:lifeskim |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C1330957 | lld:lifeskim |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C1415504 | lld:lifeskim |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C0596311 | lld:lifeskim |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
pubmed-article:12200414 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
pubmed-article:12200414 | pubmed:issue | 42 | lld:pubmed |
pubmed-article:12200414 | pubmed:dateCreated | 2002-10-15 | lld:pubmed |
pubmed-article:12200414 | pubmed:abstractText | Huntington's disease (HD) is caused by a polyglutamine expansion in the amino-terminal region of huntingtin. Mutant huntingtin is proteolytically cleaved by caspases, generating amino-terminal aggregates that are toxic for cells. The addition of calpains to total brain homogenates also leads to cleavage of wild-type huntingtin, indicating that proteolysis of mutant and wild-type huntingtin may play a role in HD. Here we report that endogenous wild-type huntingtin is promptly cleaved by calpains in primary neurons. Exposure of primary neurons to glutamate or 3-nitropropionic acid increases intracellular calcium concentration, leading to loss of intact full-length wild-type huntingtin. This cleavage could be prevented by calcium chelators and calpain inhibitors. Degradation of wild-type huntingtin by calcium-dependent proteases thus occurs in HD neurons, leading to loss of wild-type huntingtin neuroprotective activity. | lld:pubmed |
pubmed-article:12200414 | pubmed:language | eng | lld:pubmed |
pubmed-article:12200414 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12200414 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12200414 | pubmed:month | Oct | lld:pubmed |
pubmed-article:12200414 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:12200414 | pubmed:author | pubmed-author:VerderioClaud... | lld:pubmed |
pubmed-article:12200414 | pubmed:author | pubmed-author:MatteoliMiche... | lld:pubmed |
pubmed-article:12200414 | pubmed:author | pubmed-author:CattaneoElena... | lld:pubmed |
pubmed-article:12200414 | pubmed:author | pubmed-author:RigamontiDoro... | lld:pubmed |
pubmed-article:12200414 | pubmed:author | pubmed-author:ZuccatoChiara... | lld:pubmed |
pubmed-article:12200414 | pubmed:author | pubmed-author:GoffredoDonat... | lld:pubmed |
pubmed-article:12200414 | pubmed:author | pubmed-author:TartariMarzia... | lld:pubmed |
pubmed-article:12200414 | pubmed:author | pubmed-author:De... | lld:pubmed |
pubmed-article:12200414 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12200414 | pubmed:day | 18 | lld:pubmed |
pubmed-article:12200414 | pubmed:volume | 277 | lld:pubmed |
pubmed-article:12200414 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12200414 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12200414 | pubmed:pagination | 39594-8 | lld:pubmed |
pubmed-article:12200414 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:12200414 | pubmed:meshHeading | pubmed-meshheading:12200414... | lld:pubmed |
pubmed-article:12200414 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12200414 | pubmed:articleTitle | Calcium-dependent cleavage of endogenous wild-type huntingtin in primary cortical neurons. | lld:pubmed |
pubmed-article:12200414 | pubmed:affiliation | Department of Pharmacological Sciences and Center of Excellence on Neurodegenerative Diseases, University of Milan, Milano, Italy. | lld:pubmed |
pubmed-article:12200414 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12200414 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:29424 | entrezgene:pubmed | pubmed-article:12200414 | lld:entrezgene |
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