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Najjar, I.* ; Schischmanoff, P.O.* ; Baran-Marszak, F.* ; Deglesne, P.A.* ; Youlyouz-Marfak, I.* ; Pampin, M.* ; Feuillard, J.* ; Bornkamm, G.W. ; Chelbi-Alix, M.K.* ; Fagard, R.*

Novel function of STAT1β in B cells: Induction of cell death by a mechanism different from that of STAT1α.

J. Leukoc. Biol. 84, 1604-1612 (2008)
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Alternate splicing of STAT1 produces two isoforms: alpha, known as the active form, and beta, previously shown to act as a dominant-negative factor. Most studies have dealt with STAT1alpha, showing its involvement in cell growth control and cell death. To examine the specific function of either isoform in cell death, a naturally STAT1-deficient human B cell line was transfected to express STAT1alpha or STAT1beta. STAT1alpha, expressed alone, enhanced cell death, potentiated the fludarabine-induced apoptosis, and enhanced the nuclear location, the phosphorylation, and the transcriptional activity of p53. Unexpectedly, STAT1beta, expressed alone, induced cell death through a mechanism that was independent of the nuclear function of p53. Indeed, in STAT1beta-expressing B cells, p53 was strictly cytoplasmic where it formed clusters, and there was no induction of the transcriptional activity of p53. These data reveal a novel role of STAT1beta in programmed cell death, which is independent of p53.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords B lymphocytes; p53; fludarabine
ISSN (print) / ISBN 0741-5400
e-ISSN 1938-3673
Journal Journal of Leukocyte Biology
Quellenangaben Volume: 84, Issue: 6, Pages: 1604-1612 Article Number: , Supplement: ,
Publisher FASEB
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)