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JAK2 — MAPK4
Text-mined interactions from Literome
Takaoka et al., EMBO J 1999
:
Protein tyrosine kinase Pyk2 mediates the
Jak dependent
activation of
MAPK and Stat1 in IFN-gamma, but not IFN-alpha, signaling
Wang et al., Oncogene 2000
:
PD180970 did not affect
MAPK activation by PDGF or the
JAK dependent
activation of Stat3 by interleukin-6
Krasilnikov et al., Oncogene 2003
(Melanoma) :
Tyrosine phosphorylation of STAT3/5 and of JAK2 also increased upon treatment of LU1205 cells with either PD or LY, suggesting that constitutive active
MAPK and PI3K signals
inhibit tyrosine phosphorylation of
JAK/STATs
Shi et al., J Biol Chem 2004
:
Although Pyk2 has been implicated in
Janus kinase dependent activation of
MAPK and Stat1, no role for Pyk2 in the activation of other STAT proteins has been ascribed
Banes-Berceli et al., Vascul Pharmacol 2005
(Diabetes Mellitus, Experimental) :
Allopurinol ( xanthine oxidase inhibitor, 1 microM ) and l-NAME ( nitric oxide synthase inhibitor, 1 mM ) had no effect on ET-1 induced JAK2 activation, while apocynin ( NAD ( P ) H oxidase inhibitor 100 microM ) resulted in a significant inhibition of ET-1 induced
JAK2 and
MAPK activation
Ogunwobi et al., Endocrinology 2006
(Adenocarcinoma...) :
The activation of ERK and Akt but not p38
MAPK was
JAK2 dependent
Kanda et al., Endocrinology 2007
(MAP Kinase Signaling System...) :
Prolactin
induced phosphorylation of
JAK2 and ERK, whereas IFN-gamma induced phosphorylation of JAK1, JAK2, and p38
MAPK
Yung et al., Cell Signal 2008
(MAP Kinase Signaling System) :
In contrast, inhibitors of
JAK2 , phospholipase C, protein kinase C and Ca ( 2+ ) /calmodulin dependent kinase II did not
affect the ability of NGF to activate p38
MAPK
Rychli et al., Journal of thrombosis and haemostasis : JTH 2010
:
Oncostatin M (OSM) increased Ang2 expression in human umbilical vein endothelial cells via Janus kinase/signal transducer and activator of transcription (
JAK/STAT ) and
mitogen activated protein ( MAP ) kinase activation
Winston et al., J Biol Chem 1995
:
JAK2 , Ras, and Raf are
required for activation of extracellular signal regulated
kinase/mitogen activated protein kinase by growth hormone ... We have used a transient transfection system in 293 cells to evaluate the
requirement for
JAK2 in the activation of
ERK2/MAPK by GH ... We found that
JAK2 is
required for GH-simulated activation of
ERK2/MAPK ... Employing the transient expression of dominant negative forms of H-Ras and Raf-1, we determined that the
GHR/JAK2 mediated activation of
ERK2/MAPK is dependent on both Ras and Raf
Pratt et al., J Biol Chem 1996
:
Several downstream signaling events induced by GM-CSF stimulation have been described, including activation of tyrosine kinases and tyrosine phosphorylation of cellular proteins ( including beta c ) and
activation of the
Ras/mitogen activated protein kinase and the
JAK/STAT pathways
Schiemann et al., J Biol Chem 1997
:
Coexpression of dominant negative
Jak2 inhibited chimeric receptor stimulated
MAPK activity by approximately 70 %, while expression of dominant negative Ras completely blocked MAPK activation by either receptor polypeptide