◀ Back to RAF1
JAK1 — RAF1
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
RAF1
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JAK1
(directlyIncreases, JAK1 Activity, RAF1 Activity)
Evidence: It is in the cell membrane where Ras cycles between inactive guanosine diphosphate-bound and active guanosine triphosphate (GTP) -bound states, thereby activating a series of effector kinases that phosphorylate a cascade of signaling proteins.58 Ras mutants exhibit slightly less intrinsic GTPase activity than wild-type Ras; however, the principal consequence of the mutated proteins is a marked decrease in interactions between Ras and its GTPase activator protein.59 Instead of reverting to its in...
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OpenBEL Selventa BEL large corpus:
RAF1
→
JAK1
(directlyIncreases, RAF1 Activity)
Evidence: Y341 is phosphorylated by the Src family of non-RTKs, Janus kinase, and erythropoietin.
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NCI Pathway Database IL2-mediated signaling events:
RAF1 (RAF1)
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IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, activates)
Blanchard et al., Oncogene 2000, Lundin Brockdorff et al., Cytokine 2002, Karnitz et al., Mol Cell Biol 1995
Evidence: mutant phenotype, other species
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NCI Pathway Database SHP2 signaling:
RAF1 (RAF1)
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IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, activates)
Blanchard et al., Oncogene 2000, Lundin Brockdorff et al., Cytokine 2002, Karnitz et al., Mol Cell Biol 1995
Evidence: mutant phenotype
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
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Therefore,
JAK1 activity may be
involved in activation of
Raf-1 and ERK1 via G proteins activated by C5b-9
Kim et al., Biochem Biophys Res Commun 2001
:
Here, based on the recent finding of HBx ( X-gene product of hepatitis B virus ) as the inducer of Jak1, we investigated the mechanism for the HBx mediated host cell regulation and found that ( i ) HBx associates specifically with Jak1 in vivo ; ( ii ) HBx itself forms a dimer which leads to juxtaposition of associated Jak1 and subsequent activation of the tyrosine kinase activity of Jak1 ; ( iii ) HBx mediated activation of the promoters containing AP-1-, NF-kappaB-, SRE-, and SIE-sites is dependent on the activation of Jak1 ; ( iv )
Jak1 , once activated by HBx, induces Ras activity through recruitment of Grb2 and
induces tyrosine phosphorylation of
Raf1 , but not shc
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
Stancato et al., Mol Cell Biol 1997
:
Therefore, it appears that
Jak1 is
required for
Raf-1 activation by both IFN-beta and OSM
Sakatsume et al., J Biol Chem 1998
:
Interferon gamma activation of
Raf-1 is
Jak1 dependent and p21ras independent