Novel function of STAT1beta in B cells: induction of cell death by a mechanism different from that of STAT1alpha.
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.
Najjar
Imen
I
Université Paris 13, EA 3406, Service de biochimie, APHP, Hôpital Avicenne, Cedex, France.
Schischmanoff
Pierre Olivier
PO
Baran-Marszak
Fanny
F
Deglesne
Pierre-Antoine
PA
Youlyouz-Marfak
Ibtissam
I
Pampin
Mathieu
M
Feuillard
Jean
J
Bornkamm
Georg W
GW
Chelbi-Alix
Mounira K
MK
Fagard
Remi
R