| pubmed-article:15033169 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C0000098 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C0217250 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C1099354 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C0282151 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C0011164 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C0597304 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
| pubmed-article:15033169 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
| pubmed-article:15033169 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:15033169 | pubmed:dateCreated | 2004-3-22 | lld:pubmed |
| pubmed-article:15033169 | pubmed:abstractText | The cellular mechanisms underlying the neurodegenerative process in Parkinson's disease are not well understood. Using RNA interference (RNAi), we demonstrate that caspase-3-dependent proteolytic activation of protein kinase Cdelta (PKCdelta) contributes to the degenerative process in dopaminergic neurons. The Parkinsonian toxin MPP(+) activated caspase-3 and proteolytically cleaved PKCdelta into catalytic and regulatory subunits, resulting in persistent kinase activation in mesencephalic dopaminergic neuronal cells. The caspase-3 inhibitor Z-DEVD-FMK and the caspase-9 inhibitor Z-LEHD-FMK effectively blocked MPP(+)-induced PKCdelta proteolytic activation. To characterize the functional role of PKCdelta activation in MPP(+)-induced dopaminergic cell death, RNAi-mediated gene knockdown was performed. Among four siRNAs designed against PKCdelta, two specifically suppressed PKCdelta expression. The application of siRNA abolished the MPP(+)-induced PKCdelta activation, DNA fragmentation, and tyrosine hydroxylase (TH)-positive neuronal loss. Together, these results suggest that proteolytic activation of PKCdelta may be a critical downstream event in the degenerative process of Parkinson's disease. | lld:pubmed |
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| pubmed-article:15033169 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15033169 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15033169 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15033169 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15033169 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:15033169 | pubmed:issn | 1044-7431 | lld:pubmed |
| pubmed-article:15033169 | pubmed:author | pubmed-author:AnantharamVel... | lld:pubmed |
| pubmed-article:15033169 | pubmed:author | pubmed-author:KaulSiddharth... | lld:pubmed |
| pubmed-article:15033169 | pubmed:author | pubmed-author:KanthasamyAnu... | lld:pubmed |
| pubmed-article:15033169 | pubmed:author | pubmed-author:YangYongjieY | lld:pubmed |
| pubmed-article:15033169 | pubmed:author | pubmed-author:ZhangDanhuiD | lld:pubmed |
| pubmed-article:15033169 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15033169 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:15033169 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15033169 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15033169 | pubmed:pagination | 406-21 | lld:pubmed |
| pubmed-article:15033169 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:15033169 | pubmed:meshHeading | pubmed-meshheading:15033169... | lld:pubmed |
| pubmed-article:15033169 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15033169 | pubmed:articleTitle | Suppression of caspase-3-dependent proteolytic activation of protein kinase C delta by small interfering RNA prevents MPP+-induced dopaminergic degeneration. | lld:pubmed |
| pubmed-article:15033169 | pubmed:affiliation | Parkinson's Disorder Research Laboratory, Department of Biomedical Sciences, Iowa State University, Ames, IA 50011-1250, USA. | lld:pubmed |
| pubmed-article:15033169 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15033169 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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