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JAK2 — RAF1
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
RAF1
—
JAK2
(direct interaction, pull down)
Xia et al., Proc Natl Acad Sci U S A 1996*
-
IRef Hprd Interaction:
RAF1
—
JAK2
(in vitro)
Mason et al., EMBO J 1999, Xing et al., J Biol Chem 2001*, Xia et al., Proc Natl Acad Sci U S A 1996*, Cutler et al., Proc Natl Acad Sci U S A 1998*
-
IRef Hprd Interaction:
RAF1
—
JAK2
(in vivo)
Mason et al., EMBO J 1999, Xing et al., J Biol Chem 2001*, Xia et al., Proc Natl Acad Sci U S A 1996*, Cutler et al., Proc Natl Acad Sci U S A 1998*
-
IRef Ophid Interaction:
RAF1
—
JAK2
(aggregation, confirmational text mining)
Xia et al., Proc Natl Acad Sci U S A 1996*
-
IRef Ophid Interaction:
RAF1
—
JAK2
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Niculescu et al., Immunopharmacology 1999
:
Therefore,
JAK1 activity may be
involved in activation of
Raf-1 and ERK1 via G proteins activated by C5b-9
Reiterer et al., Cell cycle (Georgetown, Tex.) 2010
(Genomic Instability) :
GW5074 also inhibited JAK inhibitor induced appearance of nuclear phosphorylated
RAF-1 ( pS621RAF ) and MEK ; and it
inhibited the
JAK inhibitor induced co-immunoprecipitation of nuclear RAF-1 and MEK
Yang et al., Am J Pathol 2013
(Ischemia...) :
In mechanistic studies,
Jak2 deficiency
attenuated Raf-1/MEK1 signaling, which then reduced activity of Sp-1, an essential transcription factor responsible for eNOS expression
Xia et al., Proc Natl Acad Sci U S A 1996
:
The cytokine activated tyrosine kinase
JAK2 activates
Raf-1 in a p21ras dependent manner ... In the baculovirus coexpression system,
Raf-1 was
activated by
JAK2 in the presence of p21ras ... In contrast, in the absence of p21ras, coexpression of
JAK2 and Raf-1
resulted in an overall decrease in the
Raf-1 kinase activity
Marrero et al., J Biol Chem 1997
:
Our results indicate that : 1 ) STAT proteins play an essential role in angiotensin II-induced vascular smooth muscle cell proliferation, 2 ) JAK2 plays an essential role in the tyrosine phosphorylation of
Raf-1 , and 3 ) convergent mitogenic signaling cascades
involving the cytosolic kinases
JAK2 , MEK1, and ERK1 mediate vascular smooth muscle cell proliferation in response to both growth factor and G protein coupled receptors