Source:http://linkedlifedata.com/resource/pubmed/id/15685448
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2005-7-12
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pubmed:abstractText |
Expression of an interferon inducible gene 6-16, G1P3, increases not only in type I interferon-treated cells but also in human senescent fibroblasts. However, the function of 6-16 protein is unknown. Here we report that 6-16 is 34 kDa glycosylated protein and localized at mitochondria. Interestingly, 6-16 is expressed at high levels in gastric cancer cell lines and tissues. One of exceptional gastric cancer cell line, TMK-1, which do not express detectable 6-16, is sensitive to apoptosis induced by cycloheximide (CHX), 5-fluorouracil (5-FU) and serum-deprivation. Ectopic expression of 6-16 gene restored the induction of apoptosis and inhibited caspase-3 activity in TMK-1 cells. Thus 6-16 protein has anti-apoptotic function through inhibiting caspas-3. This anti-apoptotic function is expressed through inhibition of the depolarization of mitochondrial membrane potential and release of cytochrome c. By two-hybrid screening, we found that 6-16 protein interacts with calcium and integrin binding protein, CIB/KIP/Calmyrin (CIB), which interacts with presenilin 2, a protein involved in Alzheimer's disease. These protein interactions possibly play a pivotal role in the regulation of apoptosis, for which further detailed analyses are need. These results overall indicate that 6-16 protein may have function as a cell survival protein by inhibiting mitochondrial-mediated apoptosis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0340-7004
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pubmed:author |
pubmed-author:BarrettJ CarlJC,
pubmed-author:IdeToshinoriT,
pubmed-author:IshiharaHirotoH,
pubmed-author:KannoMasamotoM,
pubmed-author:MatsuzakiTakeshiT,
pubmed-author:NakaKazuhitoK,
pubmed-author:TaharaEiichiE,
pubmed-author:TaharaEijiEJr,
pubmed-author:TaharaHidetoshiH,
pubmed-author:TakedaYayoiY,
pubmed-author:YamazakiRyutaR,
pubmed-author:YasuiWataruW
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pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
729-40
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15685448-Apoptosis,
pubmed-meshheading:15685448-Blotting, Northern,
pubmed-meshheading:15685448-Cell Survival,
pubmed-meshheading:15685448-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:15685448-Humans,
pubmed-meshheading:15685448-Membrane Potentials,
pubmed-meshheading:15685448-Mitochondria,
pubmed-meshheading:15685448-Mitochondrial Proteins,
pubmed-meshheading:15685448-Proteins,
pubmed-meshheading:15685448-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15685448-Stomach Neoplasms,
pubmed-meshheading:15685448-Tumor Cells, Cultured
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pubmed:year |
2005
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pubmed:articleTitle |
G1P3, an interferon inducible gene 6-16, is expressed in gastric cancers and inhibits mitochondrial-mediated apoptosis in gastric cancer cell line TMK-1 cell.
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pubmed:affiliation |
Department of Cellular and Molecular Biology, Division of Integerated Medical Science, Graduate School of Biomedical Science, Hiroshima University, 1-2-3 Kasumi, Minamiku-ku, Hiroshima 734-8551, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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