کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1932865 | 1050595 | 2009 | 5 صفحه PDF | دانلود رایگان |
We have previously shown that Janus kinase 3, a member of the family of non-receptor protein tyrosine kinases, plays a critical role in the regulation of FcεRI-mediated mast cell responses. In the current study, we investigated the role of another JAK family member, JAK2, in these responses. Our results show that the treatment of IgE-sensitized mouse mast cells with an inhibitor of JAK2 (AG490) blocked the release of leukotriene C4 in a dose-dependent fashion after antigen challenge. However, prostaglandin PG D2 production and degranulation were not affected under identical experimental conditions. Transfection of RBL-2H3 mast cells with JAK-2 specific small interfering RNA resulted in a 50% reduction of LTC4 release in response to FcεRI crosslinking, but did not inhibit mast cell degranulation or calcium ionophore-induced LTC4 release, indicating involvement of JAK2 in IgE receptor-mediated leukotriene release. Taken together, these data suggest that JAK2 is a critical regulator of IgE/antigen-induced production of LTC4 in mast cells.
Journal: Biochemical and Biophysical Research Communications - Volume 390, Issue 3, 18 December 2009, Pages 786–790