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Issue 1010 coverApoptosis from Signaling Pathways to Therapeutic Tools Volume 1010 published December 2003
Ann. N.Y. Acad. Sci. 1010: 225–231 (2003). doi: 10.1196/annals.1299.040
Copyright © 2003 by the New York Academy of Sciences
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Articles by BIERBAUM, H.
Articles by ANGEL, P.
Early Activation and Induction of Apoptosis in T Cells Is Independent of c-Fos

HANNA BIERBAUMa, SVEN BAUMANNb, INGRID HERRc, JAN P. TUCKERMANNd, JOCHEN HESSa, MARINA SCHORPP-KISTNERa AND PETER ANGELa

aDivision of Signal Transduction and Growth Control, bTumor Immunology Program, cDivision of Pediatric Oncology, dDivision of Molecular Biology of the Cell I, Deutsches Krebsforschungszentrum Heidelberg, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany

Address for correspondence: Marina Schorpp-Kistner, Division of Signal Transduction and Growth Control, Deutsches Krebsforschungszentrum Heidelberg, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany. Voice: 49-6221-42-4575; fax: 49-6221-42-4554. marina.schorpp{at}dkfz.de
Ann. N.Y. Acad. Sci. 1010: 225-231 (2003).

We used c-Fos-deficient activated T cells from the spleen and c-Fos-deficient thymocytes to address the capacity of these cells to undergo apoptosis in response to various stimuli. To determine the role of c-Fos in apoptosis regulation in thymocytes, we challenged thymocytes from wild-type and c-Fos-deficient mice with either TPA or the glucocorticoid dexamethasone. After various time points cells were stained according to the Nicoletti method and analyzed by FACS. Thymocytes from both genotypes exhibited similar efficiency of apoptosis in response to treatment with TPA or dexamethasone. Our data provide clear evidence that c-Fos is not required for apoptosis regulation in activated T cells as well as in thymocytes.

Key Words: c-Fos • apoptosis • early activation • induction • T cells




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