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Novel function of STAT1β in B cells: induction of cell death by a mechanism different from that of STAT1α
Author(s) -
Najjar Imen,
Schischmanoff Pierre Olivier,
BaranMarszak Fanny,
Deglesne PierreAntoine,
YoulyouzMarfak Ibtissam,
Pampin Mathieu,
Feuillard Jean,
Bornkamm Georg W.,
ChelbiAlix Mounira K.,
Fagard Remi
Publication year - 2008
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0508287
Subject(s) - biology , programmed cell death , stat1 , apoptosis , microbiology and biotechnology , transfection , cell culture , cell growth , cancer research , phosphorylation , genetics
Alternate splicing of STAT1 produces two isoforms: α, known as the active form, and β, previously shown to act as a dominant‐negative factor. Most studies have dealt with STAT1α, 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 STAT1α or STAT1β. STAT1α, expressed alone, enhanced cell death, potentiated the fludarabine‐induced apoptosis, and enhanced the nuclear location, the phosphorylation, and the transcriptional activity of p53. Unexpectedly, STAT1β, expressed alone, induced cell death through a mechanism that was independent of the nuclear function of p53. Indeed, in STAT1β‐expressing B cells, p53 was stricktly cytoplasmic where it formed clusters, and there was no induction of the transcriptional activity of p53. These data reveal a novel role of STAT1β in programmed cell death, which is independent of p53.