In:
Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 84, No. 6 ( 2008-12-01), p. 1604-1612
Kurzfassung:
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.
Materialart:
Online-Ressource
ISSN:
0741-5400
,
1938-3673
Sprache:
Englisch
Verlag:
Oxford University Press (OUP)
Publikationsdatum:
2008
ZDB Id:
2026833-6
SSG:
12
