pubmed-article:14630083 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0020094 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C1335960 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0229664 | lld:lifeskim |
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pubmed-article:14630083 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0013081 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0205160 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0805732 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0162493 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C1366753 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C1335283 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C1150611 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0182953 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C0205548 | lld:lifeskim |
pubmed-article:14630083 | lifeskim:mentions | umls-concept:C1548425 | lld:lifeskim |
pubmed-article:14630083 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:14630083 | pubmed:dateCreated | 2003-11-21 | lld:pubmed |
pubmed-article:14630083 | pubmed:abstractText | Adult T-cell leukemia (ATL) is an aggressive malignancy that is associated with human T-cell lymphotropic virus I (HTLV-I) infection. HTLV-I transformed T-cell lines and fresh ATL cells are characterized by constitutive activation of the interleukin-2 receptor (IL-2R) signaling pathway however, the mechanism(s) responsible for constitutive IL-2R activation are unknown. To further examine the cause of this signaling pathway deregulation, we measured mRNA and protein expression levels by real-time PCR and Western blots, respectively, of four negative regulators of the IL-2R signaling pathway including src homology 2 (SH2)-containing phosphatase (SHP1), cytokine-inducible (CIS) SH2-containing protein, suppressor of cytokine signaling-1 (SOCS1) and protein inhibitor of activated signal transducer and activator of transcription 3 (STAT3) (PIAS3) in six HTLV-1 negative and seven HTLV-1 positive T-cell leukemia lines. The activation status of the JAK/STAT pathway was also examined. SHP1 mRNA and protein expression levels were selectively down regulated in all HTLV-1-infected transformed cell lines, while CIS, SOCS1, and PIAS3 protein expression were markedly but variably upregulated and the cells showed evidence of constitutive STAT3 activation. In acutely HTLV-1 infected primary CD4+ T-cells there was a gradual loss of SHP1 expression over 10 weeks in culture which correlated with progression from immortalization to transformation and loss of IL-2 dependence for growth. Two transformed cell lines that were established following HTLV-1 infection showed loss of SHP1 expression and overexpression of CIS, SOCS1, PIAS3. However, this overexpression was not adequate to block constitutive activation of the JAK/STAT pathway. Thus, multiple levels of IL-2 receptor signal deregulation are found in HTLV-1 transformed cells, which may be a result of early loss of SHP1 expression. | lld:pubmed |
pubmed-article:14630083 | pubmed:language | eng | lld:pubmed |
pubmed-article:14630083 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14630083 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:14630083 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14630083 | pubmed:month | Jan | lld:pubmed |
pubmed-article:14630083 | pubmed:issn | 0145-2126 | lld:pubmed |
pubmed-article:14630083 | pubmed:author | pubmed-author:ZhangDongshen... | lld:pubmed |
pubmed-article:14630083 | pubmed:author | pubmed-author:ZhouChanghong... | lld:pubmed |
pubmed-article:14630083 | pubmed:author | pubmed-author:MarascoWayne... | lld:pubmed |
pubmed-article:14630083 | pubmed:author | pubmed-author:ChengJihuaJ | lld:pubmed |
pubmed-article:14630083 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14630083 | pubmed:volume | 28 | lld:pubmed |
pubmed-article:14630083 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14630083 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14630083 | pubmed:pagination | 71-82 | lld:pubmed |
pubmed-article:14630083 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:14630083 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:14630083 | pubmed:articleTitle | Down-regulation of SHP1 and up-regulation of negative regulators of JAK/STAT signaling in HTLV-1 transformed cell lines and freshly transformed human peripheral blood CD4+ T-cells. | lld:pubmed |
pubmed-article:14630083 | pubmed:affiliation | Department of Cancer Immunology & AIDS, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA. | lld:pubmed |
pubmed-article:14630083 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:14630083 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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