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Publication : Biologic consequences of Stat1-independent IFN signaling.

First Author  Gil MP Year  2001
Journal  Proc Natl Acad Sci U S A Volume  98
Issue  12 Pages  6680-5
PubMed ID  11390995 Mgi Jnum  J:81243
Mgi Id  MGI:2448426 Doi  10.1073/pnas.111163898
Citation  Gil MP, et al. (2001) Biologic consequences of Stat1-independent IFN signaling. Proc Natl Acad Sci U S A 98(12):6680-5
abstractText  Although Stat1 is required for many IFN-dependent responses, recent work has shown that IFNgamma functions independently of Stat1 to affect the growth of tumor cells or immortalized fibroblasts. We now demonstrate that both IFNgamma and IFNalpha/beta regulate proliferative responses in cells of the mononuclear phagocyte lineage derived from Stat1-null mice. Using both representational difference analysis and gene arrays, we show that IFNgamma exerts its Stat1-independent actions on mononuclear phagocytes by regulating the expression of many genes. This result was confirmed by monitoring changes in expression and function of the corresponding gene products. Regulation of the expression of these genes requires the IFNgamma receptor and Jak1. The physiologic relevance of IFN-dependent, Stat1-independent signaling was demonstrated by monitoring antiviral responses in Stat1-null mice. Thus, the IFN receptors engage alternative Stat1-independent signaling pathways that have important physiological consequences.
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