| First Author | Sur R | Year | 2009 |
| Journal | Biochem Biophys Res Commun | Volume | 390 |
| Issue | 3 | Pages | 786-90 |
| PubMed ID | 19835845 | Mgi Jnum | J:155611 |
| Mgi Id | MGI:4414879 | Doi | 10.1016/j.bbrc.2009.10.050 |
| Citation | Sur R, et al. (2009) Role of Janus kinase-2 in IgE receptor-mediated leukotriene C4 production by mast cells. Biochem Biophys Res Commun 390(3):786-90 |
| abstractText | 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 FcepsilonRI-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 C(4) in a dose-dependent fashion after antigen challenge. However, prostaglandin PG D(2) 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 LTC(4) release in response to FcepsilonRI crosslinking, but did not inhibit mast cell degranulation or calcium ionophore-induced LTC(4) 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 LTC(4) in mast cells. |
