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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0013081,
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0034790,
umls-concept:C0086427,
umls-concept:C0185117,
umls-concept:C0332307,
umls-concept:C0439097,
umls-concept:C0439098,
umls-concept:C0699040,
umls-concept:C1292733,
umls-concept:C1413223,
umls-concept:C1547348,
umls-concept:C1705241,
umls-concept:C1719914,
umls-concept:C2828406,
umls-concept:C2911684
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pubmed:issue |
7
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pubmed:dateCreated |
1990-10-17
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pubmed:abstractText |
Infection and transformation by human T cell leukemia virus type I (HTLV-I) up-regulates expression of several inducible genes including those coding for cytokines involved in the proliferation of normal and leukemic T cells. We demonstrate that HTLV-I can also shut off expression of the CD3-gamma, delta, epsilon, and zeta genes that code for the constant elements of the TCR for Ag. In addition, the T cell-specific CD3-epsilon enhancer was found to be inactive in a HTLV-I-infected T cell clone. This HTLV-I-infected T cell clone (827-p19-II) that could be cultured in the absence of IL-2 lacked the CD3 proteins but did express the TCR-alpha and -beta proteins intracellularly. In the absence of the CD3-gamma, delta, epsilon, and zeta polypeptide chains the disulfide bridged TCR-alpha/beta heterodimer was not formed and the Ag receptor did not appear at the cell surface. These results allowed two major conclusions: first, HTLV-I infection has an effect on the T cell specific regulatory elements that coordinately regulate CD3-gamma, delta, epsilon, and zeta expression and second, the CD3-gamma, delta, epsilon, and zeta proteins are necessary for formation and routing the variable TCR-alpha/beta (or -gamma/delta) heterodimer to the human T cell surface.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Macromolecular Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
145
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2297-303
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:2144550-Antigens, CD3,
pubmed-meshheading:2144550-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:2144550-Blotting, Northern,
pubmed-meshheading:2144550-Blotting, Southern,
pubmed-meshheading:2144550-Cell Line,
pubmed-meshheading:2144550-Cell Membrane,
pubmed-meshheading:2144550-Down-Regulation,
pubmed-meshheading:2144550-Enhancer Elements, Genetic,
pubmed-meshheading:2144550-Gene Expression Regulation,
pubmed-meshheading:2144550-HTLV-I Infections,
pubmed-meshheading:2144550-Human T-lymphotropic virus 1,
pubmed-meshheading:2144550-Humans,
pubmed-meshheading:2144550-Macromolecular Substances,
pubmed-meshheading:2144550-Receptors, Antigen, T-Cell
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pubmed:year |
1990
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pubmed:articleTitle |
Human T cell leukemia virus type I prevents cell surface expression of the T cell receptor through down-regulation of the CD3-gamma, -delta, -epsilon, and -zeta genes.
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pubmed:affiliation |
DNAX Research Institute, Department of Human Immunology, Palo Alto CA 94304-1104.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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