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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2005-4-8
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pubmed:databankReference |
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pubmed:abstractText |
MSSP has been identified as a transcription factor that regulates the c-myc gene. MSSP was later found to positively or negatively regulate a variety of genes, including alpha-smooth actin, MHC class I, MHC class 2 and the thyrotropin receptor. The knockout mice for the Mssp gene developed by us revealed that these mice became partially embryonic lethal due to a low concentration of progesterone at E2.5. In this study, we further analyzed Mssp-knockout mice and found that the expression of the Fas gene was repressed, resulting in abrogation of Fas-mediated induction of apoptosis both in Mssp-knockout mice and primary thymocytes. MSSP was then found to stimulate promoter activity of the Fas gene by binding to a region spanning -1035 to -635 in chromatin immunoprecipitation assays. Binding of MSSP in the MSSP-binding sequence, TCTAAT, located in this region was confirmed by mobility shift assays, and deletion of this sequence from the Fas promoter was found to result in loss of MSSP-dependent stimulating activity. The results suggest that MSSP is an important mediator for Fas-induced apoptosis in vivo and in vitro.
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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/Antigens, CD164,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Cd164 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Fas protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0014-4827
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
305
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
324-32
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15817157-Animals,
pubmed-meshheading:15817157-Antigens, CD164,
pubmed-meshheading:15817157-Antigens, CD95,
pubmed-meshheading:15817157-Apoptosis,
pubmed-meshheading:15817157-Chromatin Immunoprecipitation,
pubmed-meshheading:15817157-DNA-Binding Proteins,
pubmed-meshheading:15817157-Down-Regulation,
pubmed-meshheading:15817157-Gene Expression Regulation,
pubmed-meshheading:15817157-Genes, Reporter,
pubmed-meshheading:15817157-Humans,
pubmed-meshheading:15817157-Luciferases,
pubmed-meshheading:15817157-Mice,
pubmed-meshheading:15817157-Mice, Knockout,
pubmed-meshheading:15817157-Molecular Sequence Data,
pubmed-meshheading:15817157-Promoter Regions, Genetic,
pubmed-meshheading:15817157-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:15817157-Sequence Deletion,
pubmed-meshheading:15817157-Thymus Gland,
pubmed-meshheading:15817157-Transcription Factors
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pubmed:year |
2005
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pubmed:articleTitle |
Positive regulation of Fas gene expression by MSSP and abrogation of Fas-mediated apoptosis induction in MSSP-deficient mice.
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pubmed:affiliation |
Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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