pubmed-article:11498280 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11498280 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:11498280 | lifeskim:mentions | umls-concept:C0030011 | lld:lifeskim |
pubmed-article:11498280 | lifeskim:mentions | umls-concept:C1417014 | lld:lifeskim |
pubmed-article:11498280 | lifeskim:mentions | umls-concept:C1522240 | lld:lifeskim |
pubmed-article:11498280 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:11498280 | lifeskim:mentions | umls-concept:C1998548 | lld:lifeskim |
pubmed-article:11498280 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:11498280 | pubmed:dateCreated | 2001-8-10 | lld:pubmed |
pubmed-article:11498280 | pubmed:abstractText | Methylglyoxal (MG) is a physiological metabolite, but it is known to be toxic, inducing stress and causing apoptosis. Our previous studies demonstrated that MG induced apoptosis in Jurkat cells by activating the c-Jun N-terminal kinase (JNK) signal transduction pathway, which induced an obvious decrease in mitochondrial membrane potential, followed by caspase-3 activation. Here, we observed that MG-induced apoptosis was associated with both rapid production of superoxide anion (O(2)(-)) followed by a marked increase in ROS and striking and temporal activation of ASK1. Overexpression of wild-type ASK1 could enhance the rate of apoptosis induced by MG, whereas the expression of the kinase-inactive form of ASK1 notably prevented cells from MG-induced death. NAC and PDTC blocked the activation of ASK1 and MG-induced apoptosis completely. Moreover, nonthiol antioxidants SOD-mimic MnTBAP and catalase together obviously inhibited MG-induced ASK1 activation and apoptosis induction. Correspondingly, MG-mediated ASK1 activation was enhanced by diethyldithiocarbamate (DDC). Addition of antioxidant into the culture of cells at a later stage (4-8 h after the initial MG treatment) failed to prevent their death. These results suggest that activating ASK1 at the early stage linking to production of O(2)(-) is crucial for subsequent progression of apoptosis in MG-treated Jurkat cells. | lld:pubmed |
pubmed-article:11498280 | pubmed:language | eng | lld:pubmed |
pubmed-article:11498280 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11498280 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11498280 | pubmed:month | Aug | lld:pubmed |
pubmed-article:11498280 | pubmed:issn | 0891-5849 | lld:pubmed |
pubmed-article:11498280 | pubmed:author | pubmed-author:SuzukiHH | lld:pubmed |
pubmed-article:11498280 | pubmed:author | pubmed-author:NakashimaII | lld:pubmed |
pubmed-article:11498280 | pubmed:author | pubmed-author:MiyataTT | lld:pubmed |
pubmed-article:11498280 | pubmed:author | pubmed-author:YokoyamaTT | lld:pubmed |
pubmed-article:11498280 | pubmed:author | pubmed-author:NagaseFF | lld:pubmed |
pubmed-article:11498280 | pubmed:author | pubmed-author:EMSS | lld:pubmed |
pubmed-article:11498280 | pubmed:author | pubmed-author:TaiYY | lld:pubmed |
pubmed-article:11498280 | pubmed:author | pubmed-author:AkhandA AAA | lld:pubmed |
pubmed-article:11498280 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11498280 | pubmed:day | 15 | lld:pubmed |
pubmed-article:11498280 | pubmed:volume | 31 | lld:pubmed |
pubmed-article:11498280 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11498280 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11498280 | pubmed:pagination | 469-78 | lld:pubmed |
pubmed-article:11498280 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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pubmed-article:11498280 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11498280 | pubmed:articleTitle | Superoxide-mediated early oxidation and activation of ASK1 are important for initiating methylglyoxal-induced apoptosis process. | lld:pubmed |
pubmed-article:11498280 | pubmed:affiliation | Department of Immunology, Nagoya University School of Medicine, Aichi, Japan. | lld:pubmed |
pubmed-article:11498280 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11498280 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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