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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