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Inhibition of Activation of Transcription Factor Ap-1 by Cd28 Signaling
Division of Immunochemistry, Deutsches Krebsforschungszentrum, Heidelberg, Germany..
Division of Immunochemistry, Deutsches Krebsforschungszentrum, Heidelberg, Germany..
Division of Immunochemistry, Deutsches Krebsforschungszentrum, Heidelberg, Germany..
1994 (English)In: Biochemical Journal, ISSN 0264-6021, E-ISSN 1470-8728, Vol. 302, 119-123 p.Article in journal (Refereed) Published
Abstract [en]

Co-stimulation of T-lymphocytes by T-cell receptor (TcR) occupancy and activation of the CD28 surface molecule results in enhanced proliferation and interleukin 2 (IL-2) production. The increase in IL-2 gene expression triggered by CD28 involves a KB-like sequence in the 5'-regulatory region of the IL-2 promoter, called CD28-responsive element. Stimulation of T-cells by agonistic anti-CD28 antibodies in conjunction with phorbol 12-myristate 13-acetate (PMA)- or TcR-derived signals induces the enhanced activation of the transcription factor NF-B-K. Here we report that CD28 engagement, however, exerts opposite effects on the transcription factor AP-1. Whereas anti-CD28 together with PMA increased the DNA binding and trans-activation activity of NF-B-K, PMA-induced activation of AP-1 was significantly suppressed. The inhibitory effect exerted by anti-CD38 was observed at the level of DNA binding as well as in functional reporter-gene assays. These results suggest that the two transcription factors are independently regulated and may perform different functions during T-cell activation.

Place, publisher, year, edition, pages
1994. Vol. 302, 119-123 p.
Keyword [en]
antigen, c-fos, death, expression, interleukin-2 gene, lymphocytes, nf-kappa-b, pathway, phosphorylation, receptor
National Category
Cell Biology Biochemistry and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-87083ISI: A1994PC82800017OAI: oai:DiVA.org:liu-87083DiVA: diva2:584850
Available from: 2013-01-09 Created: 2013-01-09 Last updated: 2017-12-06

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Los, Marek Jan

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