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Stimulation of interferon regulatory factor-1 by prolactinDepartments of Medicine, Molecular and Cellular Biology, Immunology, and the Cell and Molecular Biology Program, Baylor College of Medicine, Houston, Texas, USA; Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USAyulee{at}bcm.tmc.edu Prolactin (PRL), a pituitary peptide hormone, is known to regulate diverse cellular functions including proliferation, differentiation, angiogenesis and protection against apoptosis and inflammation. To understand the mechanism of PRL signaling in T cells, we have cloned both PRL and its receptor (PRL-R), one potent mediator of PRL signaling, Stat5b, and a panel of PRL-inducible immediate early genes from T cells. We are employing these genes as tools with which to understand how PRL regulates the expression of one target gene, the transcription factor interferon regulatory factor-1 (IRF-1), which is a multifunctional immune regulator gene. In investigating regulatory events along the PRL-R/JAK/Stat/IRF-1 signaling pathway, we show that Stat factors can activate as well as inhibit IRF-1 promoter activity and that cross-talk between Stat and NFkB signaling pathways also regulates IRF-1 promoter activity. These findings have much broader implications not only for T lymphocytes but also for other PRL responsive target cells and tissues.
Key Words: PRL • Stat • NFkB • IRF-1 • T cells • immune response
Lupus, Vol. 10, No. 10,
691-699 (2001) This article has been cited by other articles:
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