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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
46
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pubmed:dateCreated |
2002-11-11
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pubmed:abstractText |
Oxidative stress induces JNK activation, which leads to apoptosis through mitochondria-dependent caspase activation. However, little is known about the mechanism by which JNK alters mitochondrial function. In this study, we investigated the role of phosphorylation of myeloid cell leukemia 1 (Mcl-1), an anti-apoptotic member of the Bcl-2 family, in oxidative stress-induced apoptosis. We found that JNK phosphorylated Ser-121 and Thr-163 of Mcl-1 in response to stimulation with H(2)O(2) and that transfection of unphosphorylatable Mcl-1 resulted in an enhanced anti-apoptotic activity in response to stimulation with H(2)O(2). JNK-dependent phosphorylation and thus inactivation of Mcl-1 may be one of the mechanisms through which oxidative stress induces cellular damage.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Alanine,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrogen Peroxide,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 8,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Oxygen,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoric Monoester Hydrolases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Serine,
http://linkedlifedata.com/resource/pubmed/chemical/Threonine,
http://linkedlifedata.com/resource/pubmed/chemical/myeloid cell leukemia sequence 1...,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
277
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
43730-4
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12223490-Adenoviridae,
pubmed-meshheading:12223490-Alanine,
pubmed-meshheading:12223490-Amino Acid Sequence,
pubmed-meshheading:12223490-Animals,
pubmed-meshheading:12223490-Apoptosis,
pubmed-meshheading:12223490-Binding Sites,
pubmed-meshheading:12223490-Blotting, Western,
pubmed-meshheading:12223490-Cell Line,
pubmed-meshheading:12223490-Cell Survival,
pubmed-meshheading:12223490-DNA, Complementary,
pubmed-meshheading:12223490-Escherichia coli,
pubmed-meshheading:12223490-Humans,
pubmed-meshheading:12223490-Hydrogen Peroxide,
pubmed-meshheading:12223490-Mice,
pubmed-meshheading:12223490-Mitochondria,
pubmed-meshheading:12223490-Mitogen-Activated Protein Kinase 8,
pubmed-meshheading:12223490-Mitogen-Activated Protein Kinases,
pubmed-meshheading:12223490-Molecular Sequence Data,
pubmed-meshheading:12223490-Neoplasm Proteins,
pubmed-meshheading:12223490-Oxidative Stress,
pubmed-meshheading:12223490-Oxygen,
pubmed-meshheading:12223490-Phosphoric Monoester Hydrolases,
pubmed-meshheading:12223490-Phosphorylation,
pubmed-meshheading:12223490-Plasmids,
pubmed-meshheading:12223490-Promoter Regions, Genetic,
pubmed-meshheading:12223490-Protein Binding,
pubmed-meshheading:12223490-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:12223490-Sequence Homology, Amino Acid,
pubmed-meshheading:12223490-Serine,
pubmed-meshheading:12223490-Threonine,
pubmed-meshheading:12223490-Transfection,
pubmed-meshheading:12223490-p38 Mitogen-Activated Protein Kinases
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pubmed:year |
2002
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pubmed:articleTitle |
Phosphorylation and inactivation of myeloid cell leukemia 1 by JNK in response to oxidative stress.
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pubmed:affiliation |
Laboratory of Cell Signaling, Department of Hard Tissue Engineering, Division of Bio-Matrix, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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