| pubmed-article:20346366 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20346366 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:20346366 | lifeskim:mentions | umls-concept:C0910167 | lld:lifeskim |
| pubmed-article:20346366 | lifeskim:mentions | umls-concept:C0040113 | lld:lifeskim |
| pubmed-article:20346366 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:20346366 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
| pubmed-article:20346366 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:20346366 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:20346366 | lifeskim:mentions | umls-concept:C1516044 | lld:lifeskim |
| pubmed-article:20346366 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:20346366 | pubmed:dateCreated | 2010-5-17 | lld:pubmed |
| pubmed-article:20346366 | pubmed:abstractText | In mouse thymic lymphoma 3SB cells bearing wild type p53, ionizing radiation (IR) and UV light are potent triggers of caspase-3-dependent apoptosis. Although cytochrome c was released from mitochondria as expected, caspase-9 activation was not observed in UV-exposed cells. Laser scanning confocal microscopy analysis showed that caspase-9 is localized in an unusual punctuated pattern in UV-induced apoptotic cells. In agreement with differences in the status of caspase-9 activation between IR and UV, subcellular protein fractionation experiments showed that pro-apoptotic apoptosis protease-activating factor 1 (Apaf-1), normally a part of the apoptosome assembled in response to the release of cytochrome c from mitochondria, and B-cell lymphoma extra long (Bcl-xL), an inhibitor of the change in mitochondrial membrane permeability, were redistributed by the IR-exposure but not by the UV-exposure. Instead of the sequestration of the capase-9/apoptosome activation in UV-induced apoptotic cells, the extrinsic apoptotic signaling generated by caspase-8 activation and consequent activation of B-cell lymphoma extra long (Bid) to release cytochrome c from mitochondria was observed. Thus, the post-mitochondrial apoptotic pathway downstream of cytochrome c release cannot operate the apoptosome function in UV-induced apoptosis in thymic 3SB cells. The intracellular redistribution and sequestration of apoptosis-related proteins upon mitochondrion-based apoptotic signaling was identified as a novel cellular mechanism to respond to DNA damage in an agent type-specific manner. This finding suggests that the kind of the critical ultimate apoptosis-inducing DNA lesion complex form resulting from the agent-specific DNA damage responses is important to determine which of apoptosis signals would be activated. | lld:pubmed |
| pubmed-article:20346366 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20346366 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20346366 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20346366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20346366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20346366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20346366 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20346366 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:20346366 | pubmed:issn | 0027-5107 | lld:pubmed |
| pubmed-article:20346366 | pubmed:author | pubmed-author:TatsukaMasaak... | lld:pubmed |
| pubmed-article:20346366 | pubmed:author | pubmed-author:KogaSatomiS | lld:pubmed |
| pubmed-article:20346366 | pubmed:author | pubmed-author:OkamotoMayumi... | lld:pubmed |
| pubmed-article:20346366 | pubmed:copyrightInfo | Copyright 2010 Elsevier B.V. All rights reserved. | lld:pubmed |
| pubmed-article:20346366 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:20346366 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:20346366 | pubmed:volume | 688 | lld:pubmed |
| pubmed-article:20346366 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20346366 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20346366 | pubmed:pagination | 78-87 | lld:pubmed |
| pubmed-article:20346366 | pubmed:meshHeading | pubmed-meshheading:20346366... | lld:pubmed |
| pubmed-article:20346366 | pubmed:meshHeading | pubmed-meshheading:20346366... | lld:pubmed |
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| pubmed-article:20346366 | pubmed:meshHeading | pubmed-meshheading:20346366... | lld:pubmed |
| pubmed-article:20346366 | pubmed:meshHeading | pubmed-meshheading:20346366... | lld:pubmed |
| pubmed-article:20346366 | pubmed:meshHeading | pubmed-meshheading:20346366... | lld:pubmed |
| pubmed-article:20346366 | pubmed:meshHeading | pubmed-meshheading:20346366... | lld:pubmed |
| pubmed-article:20346366 | pubmed:meshHeading | pubmed-meshheading:20346366... | lld:pubmed |
| pubmed-article:20346366 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20346366 | pubmed:articleTitle | Differential regulation of caspase-9 by ionizing radiation- and UV-induced apoptotic pathways in thymic cells. | lld:pubmed |
| pubmed-article:20346366 | pubmed:affiliation | Department of Life Sciences, Faculty of Life and Environmental Sciences, Prefectural University of Hiroshima, Shoubara, Hiroshima 727-0023, Japan. | lld:pubmed |
| pubmed-article:20346366 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20346366 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
