rdf:type |
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lifeskim:mentions |
|
pubmed:issue |
21
|
pubmed:dateCreated |
2006-10-16
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pubmed:abstractText |
Dysregulation of beta-catenin signaling has been implicated in the malignant transformation of cells. However, the role of beta-catenin in the human T-cell leukemia virus type 1 (HTLV-1)-induced transformation of T cells is unknown. Here we found that beta-catenin protein was overexpressed in the nucleus and that beta-catenin-dependent transcription was significantly enhanced in Tax-positive HTLV-1-infected T-cell lines compared to that in Tax-negative HTLV-1-infected T-cell lines. Transfection with beta-catenin-specific small interfering RNA inhibited the growth of the Tax-positive HTLV-1-infected T-cell line HUT-102. Transient transfection of Tax appeared to enhance beta-catenin-dependent transcription by stabilizing the beta-catenin protein via activation of the cyclic AMP (cAMP) response element-binding protein. HTLV-1-infected T-cell lines overexpressing beta-catenin also showed increased Akt activity via Tax activation of the cAMP response element-binding protein, resulting in the phosphorylation and inactivation of glycogen synthase kinase 3beta, which phosphorylates beta-catenin for ubiquitination. The phosphatidylinositol 3-kinase inhibitor LY294002 reduced beta-catenin expression in Tax-positive T-cell lines, and inactivation of glycogen synthase kinase 3beta by lithium chloride restored beta-catenin expression in Tax-negative T-cell lines. Finally, we showed that dominant-negative Akt inhibited Tax-induced beta-catenin-dependent transcription. These results indicate that Tax activates beta-catenin through the Akt signaling pathway. Our findings suggest that activation of beta-catenin by Tax may be important in the transformation of T cells by HTLV-1 infection.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-10733430,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-10749138,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-10921899,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-11380402,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-11420661,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-11425858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-12063252,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-12130512,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-12460931,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-12592400,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-12781368,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-12829841,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-1351105,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-15185310,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-15541474,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-21228251,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-2161813,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-2541443,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-2866223,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-2888190,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-6088403,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-8710892,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-9151835,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-9160887,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-9556553,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16920823-9710589
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CREB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, tax,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proteasome Endopeptidase Complex,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/TCF Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/beta Catenin
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-538X
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
80
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
10497-505
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pubmed:dateRevised |
2011-2-2
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pubmed:meshHeading |
pubmed-meshheading:16920823-Humans,
pubmed-meshheading:16920823-DNA,
pubmed-meshheading:16920823-Cell Transformation, Neoplastic,
pubmed-meshheading:16920823-Base Sequence,
pubmed-meshheading:16920823-DNA, Viral,
pubmed-meshheading:16920823-Models, Biological,
pubmed-meshheading:16920823-HeLa Cells,
pubmed-meshheading:16920823-Cell Line,
pubmed-meshheading:16920823-Transcription, Genetic,
pubmed-meshheading:16920823-Cell Proliferation,
pubmed-meshheading:16920823-T-Lymphocytes,
pubmed-meshheading:16920823-Signal Transduction,
pubmed-meshheading:16920823-Transfection,
pubmed-meshheading:16920823-Proteasome Endopeptidase Complex,
pubmed-meshheading:16920823-Human T-lymphotropic virus 1,
pubmed-meshheading:16920823-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:16920823-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:16920823-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:16920823-Gene Products, tax,
pubmed-meshheading:16920823-TCF Transcription Factors
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