Gene interactions and pathways from curated databases and text-mining

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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 *

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