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rdf:type |
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lifeskim:mentions |
umls-concept:C0014597,
umls-concept:C0018270,
umls-concept:C0024109,
umls-concept:C0026179,
umls-concept:C0031715,
umls-concept:C0037083,
umls-concept:C0040690,
umls-concept:C0075193,
umls-concept:C0162638,
umls-concept:C0205216,
umls-concept:C0285558,
umls-concept:C0812228,
umls-concept:C0814472,
umls-concept:C1510411,
umls-concept:C1546857,
umls-concept:C1705328,
umls-concept:C1705341,
umls-concept:C1710082,
umls-concept:C2349975
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pubmed:issue |
4
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pubmed:dateCreated |
2005-2-14
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pubmed:abstractText |
We demonstrate how co-treatment of low-dose staurosporine (STS) and TGF-beta1, which alone have little effect on cell death, markedly induces apoptosis in Mv1Lu mink lung epithelial cells, but not in its clonal variant R1B cells lacking functional TGF-beta signaling. This process was associated with mitochondria-dependent apoptosis and the enhanced TGF-beta/Smad signaling in Mv1Lu cells. When R1B cells were infected with adenovirus carrying wild-type ALK5, a functional TGF-beta type I receptor gene, the apoptotic cell death was significantly restored in these cells following co-treatment of low-dose STS and TGF-beta1. Treatment of Mv1Lu cells with both low-dose STS and TGF-beta1 decreased the activity of phospho-Akt, which is involved in cell survival signal. In addition, pre-treatments of PI3 kinase inhibitors, LY294002 and wortmannin, further increased the apoptosis of MvlLu cells induced by co-treatment of low-dose STS and TGF-beta1. And overexpression of constitutively active Akt (myr-Akt) using adenoviral expression system inhibited the apoptotic cell death of Mv1Lu cells by about 50% upon co-treatment of low-dose STS and TGF-beta1. These results suggest that co-treatment of low-dose STS and TGF-beta1 induces apoptosis of mink lung epithelial cells by enhancing TGF-beta signaling and in part suppressing cytoprotective signaling.
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0006-291X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
328
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1170-81
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15708000-Animals,
pubmed-meshheading:15708000-Apoptosis,
pubmed-meshheading:15708000-Cell Line,
pubmed-meshheading:15708000-Cell Survival,
pubmed-meshheading:15708000-Dose-Response Relationship, Drug,
pubmed-meshheading:15708000-Drug Combinations,
pubmed-meshheading:15708000-Mink,
pubmed-meshheading:15708000-Phosphorylation,
pubmed-meshheading:15708000-Protein-Serine-Threonine Kinases,
pubmed-meshheading:15708000-Proto-Oncogene Proteins,
pubmed-meshheading:15708000-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:15708000-Respiratory Mucosa,
pubmed-meshheading:15708000-Signal Transduction,
pubmed-meshheading:15708000-Staurosporine,
pubmed-meshheading:15708000-Transforming Growth Factor beta,
pubmed-meshheading:15708000-Transforming Growth Factor beta1
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pubmed:year |
2005
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pubmed:articleTitle |
Apoptosis of mink lung epithelial cells by co-treatment of low-dose staurosporine and transforming growth factor-beta1 depends on the enhanced TGF-beta signaling and requires the decreased phosphorylation of PKB/Akt.
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pubmed:affiliation |
Research Institute, National Cancer Center, Goyang, Gyeonggi 411-769, Republic of Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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