Source:http://linkedlifedata.com/resource/pubmed/id/12595531
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
18
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pubmed:dateCreated |
2003-4-28
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pubmed:abstractText |
Engagement of the T cell antigen receptor (TCR) rapidly induces multiple signal transduction pathways, including ERK activation. Here, we report a critical role for ERK at a late stage of T cell activation. Inhibition of the ERK pathway 2-6 h after the start of TCR stimulation significantly impaired interleukin-2 (IL-2) production, whereas the same treatment during the first 2 h had no effect. ERK inhibition significantly impaired nuclear translocation of c-Rel with a minimum reduction of NF-AT activity. Requirement for sustained ERK activation was also confirmed using primary T cells. To induce sustained activation of ERK, T cells required continuous engagement of TCR. Stimulation of T cells with soluble anti-TCR antibody resulted in activation of ERK lasting for 60 min, but failed to induce IL-2 production. In contrast, plate-bound anti-TCR antibody activated ERK over 4 h and induced IL-2. Furthermore, T cells treated with soluble anti-TCR antibody produced IL-2 when phorbol 12-myristate 13-acetate, which activates ERK, was present in the culture medium 2-6 h after the start of stimulation. Together, the data demonstrate the presence of a novel activation process following TCR stimulation that requires ERK-dependent regulation of c-Rel, a member of the NF-kappaB family.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-rel,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
2
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pubmed:volume |
278
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
15685-92
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12595531-Active Transport, Cell Nucleus,
pubmed-meshheading:12595531-Animals,
pubmed-meshheading:12595531-CHO Cells,
pubmed-meshheading:12595531-Cricetinae,
pubmed-meshheading:12595531-Enzyme Activation,
pubmed-meshheading:12595531-Humans,
pubmed-meshheading:12595531-Interleukin-2,
pubmed-meshheading:12595531-Jurkat Cells,
pubmed-meshheading:12595531-Lymphocyte Activation,
pubmed-meshheading:12595531-Mitogen-Activated Protein Kinases,
pubmed-meshheading:12595531-Proto-Oncogene Proteins c-rel,
pubmed-meshheading:12595531-Receptors, Antigen, T-Cell,
pubmed-meshheading:12595531-T-Lymphocytes,
pubmed-meshheading:12595531-Tetradecanoylphorbol Acetate
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pubmed:year |
2003
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pubmed:articleTitle |
A novel ERK-dependent signaling process that regulates interleukin-2 expression in a late phase of T cell activation.
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pubmed:affiliation |
Program in Molecular Immunology, Institute of Molecular Medicine and Genetics, Medical College of Georgia, CA 2004, 1120 15th Street, Augusta, GA 30912-2600, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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