| pubmed-article:19751724 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19751724 | lifeskim:mentions | umls-concept:C1882598 | lld:lifeskim |
| pubmed-article:19751724 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:19751724 | lifeskim:mentions | umls-concept:C1413109 | lld:lifeskim |
| pubmed-article:19751724 | lifeskim:mentions | umls-concept:C0054534 | lld:lifeskim |
| pubmed-article:19751724 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:19751724 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:19751724 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:19751724 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:19751724 | pubmed:dateCreated | 2009-11-20 | lld:pubmed |
| pubmed-article:19751724 | pubmed:abstractText | Calpains and caspases are cysteine endopeptidases which share many similar substrates. Caspases are essential for caspase-dependent apoptotic death where calpains may play an augmentive role, while calpains are strongly implicated in necrotic cell death morphologies. Previous studies have demonstrated a down-regulation in the expression of many components of the caspase-dependent cell death pathway during CNS development. We therefore sought to determine if there is a corresponding upregulation of calpains. The major CNS calpains are the mu-and m-isoforms, composed of the unique 80 kDa calpain 1 and 2 subunits, respectively, and the shared 28 kDa small subunit. In rat brain, relative protein and mRNA levels of calpain 1, calpain 2, caspase 3, and the endogenous calpain inhibitor-calpastatin, were evaluated using western blot and real-time RT-PCR. The developmental time points examined ranged from embryonic day 18 until postnatal day 90. Calpain 1 and calpastatin protein and mRNA levels were low at early developmental time points and increased dramatically by P30. Conversely, caspase-3 expression was greatest at E18, and was rapidly downregulated by P30. Calpain 2 protein and mRNA levels were relatively constant throughout the E18-P90 age range examined. The inverse relationship of calpain 1 and caspase 3 levels during CNS development is consistent with the shift from caspase-dependent to caspase-independent cell death mechanisms following CNS injury in neonatal vs. adult rat brain. | lld:pubmed |
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| pubmed-article:19751724 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19751724 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19751724 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19751724 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19751724 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19751724 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19751724 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19751724 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:19751724 | pubmed:issn | 1090-2430 | lld:pubmed |
| pubmed-article:19751724 | pubmed:author | pubmed-author:GeddesJames... | lld:pubmed |
| pubmed-article:19751724 | pubmed:author | pubmed-author:BondadaVimala... | lld:pubmed |
| pubmed-article:19751724 | pubmed:author | pubmed-author:LiYanzhangY | lld:pubmed |
| pubmed-article:19751724 | pubmed:author | pubmed-author:JoshiAashishA | lld:pubmed |
| pubmed-article:19751724 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19751724 | pubmed:volume | 220 | lld:pubmed |
| pubmed-article:19751724 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19751724 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19751724 | pubmed:pagination | 316-9 | lld:pubmed |
| pubmed-article:19751724 | pubmed:dateRevised | 2011-5-10 | lld:pubmed |
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| pubmed-article:19751724 | pubmed:meshHeading | pubmed-meshheading:19751724... | lld:pubmed |
| pubmed-article:19751724 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19751724 | pubmed:articleTitle | Calpain 1 and Calpastatin expression is developmentally regulated in rat brain. | lld:pubmed |
| pubmed-article:19751724 | pubmed:affiliation | Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40536-0509, USA. | lld:pubmed |
| pubmed-article:19751724 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19751724 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19751724 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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