◀ Back to IL3

IL3 — JAK1

Text-mined interactions from Literome

Subramaniam et al., Biochem Biophys Res Commun 1999 : Immunoprecipitation with specific antibodies followed by Western blot analysis with antiphosphotyrosine antibody has shown that in U937 cells, interleukin-17 induces time dependent stimulation of tyrosine phosphorylation of JAK 1 , 2 and 3, Tyk 2 and STAT 1, 2, 3 and 4 within 0.5 to 30 min. Interleukin-17 mediated tyrosine phosphorylation of these proteins strongly suggests that the JAK/STAT signaling pathway may play a major role in transducing signals from interleukin-17 receptors to the nucleus
Yu et al., Oncogene 2003 : Further biochemical analyses revealed that IL-3 induced Jak/Stat , Erk, and PI3 kinase pathways in SHP-2 ( -/- ) cells were impaired and reintroduction of WT SHP-2 into mutant cells partially restored IL-3 signaling
To et al., Br J Cancer 2004 (Cell Transformation, Neoplastic...) : The interleukin mediated Janus kinase ( JAK ) /STAT pathway plays a crucial role in carcinogenesis
Huang et al., J Cell Biochem 2005 : IL-3 induces tyrosine phosphorylation of both JAK1 and JAK2
Pecaric-Petkovic et al., Blood 2009 (Hypersensitivity) : These effects are similar to that of IL-3, but the signaling pathways engaged are distinct because IL-33 strongly activates NF-kappaB and shows a preference for p38 MAP-kinase, while IL-3 acts through Jak/Stat and preferentially activates ERK
Dorsch et al., Biochem Biophys Res Commun 1995 : Whereas phosphorylation of these proteins was induced by both cytokines, phosphorylation of Jak1 was induced only by IL-3 and not by TPO, distinguishing the signal transduction of the two cytokines on a molecular level