| pubmed-article:18676372 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0026237 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0020291 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0007745 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0037906 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0242184 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0442967 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0079411 | lld:lifeskim |
| pubmed-article:18676372 | lifeskim:mentions | umls-concept:C0128101 | lld:lifeskim |
| pubmed-article:18676372 | pubmed:issue | 39 | lld:pubmed |
| pubmed-article:18676372 | pubmed:dateCreated | 2008-9-22 | lld:pubmed |
| pubmed-article:18676372 | pubmed:abstractText | Ceramide functions as an important second messenger in apoptosis signaling pathways. In this report, we show that treatment of NT-2 neuronal precursor cells with hypoxia/reoxygenation (H/R) resulted in ceramide up-regulation. This elevation in ceramide was primarily due to the actions of acid sphingomyelinase and ceramide synthase LASS 5, demonstrating the action of the salvage pathway. Hypoxia/reoxygenation treatment led to Bax translocation from the cytoplasm to mitochondria and cytochrome c release from mitochondria. Down-regulation of either acid sphingomyelinase or LASS 5-attenuated ceramide accumulation and H/R-induced Bax translocation to mitochondria. Overall, we have demonstrated that ceramide up-regulation following H/R is pertinent to Bax activation to promote cell death. | lld:pubmed |
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| pubmed-article:18676372 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18676372 | pubmed:citationSubset | IM | lld:pubmed |
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