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