Gene interactions and pathways from curated databases and text-mining

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JAK1 — RAF1

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: RAF1 → 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...
  • 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.
  • NCI Pathway Database IL2-mediated signaling events: RAF1 (RAF1) → 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
  • NCI Pathway Database SHP2 signaling: RAF1 (RAF1) → 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 : 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