Gene interactions and pathways from curated databases and text-mining

◀ Back to JAK2

JAK2 — JAK3

Pathways - manually collected, often from reviews:

  • BioCarta il 6 signaling pathway: IL-6/IL-6/IL-6R-alpha/IL-6R-alpha/GP130/GP130/JAKS complex (JAK2_JAK1_JAK3-LRPPRC-IL6R-IL6) → JAKs (JAK2/JAK1/JAK3) (modification, collaborate)
  • BioCarta role of erbb2 in signal transduction and oncology: JAKs (JAK2/JAK1/JAK3) → IL-6/IL-6/IL-6R-alpha/IL-6R-alpha/GP130/GP130/JAKs complex (IL6-IL6R-LRPPRC-JAK2_JAK1_JAK3) (modification, collaborate)
  • BioCarta stat3 signaling pathway: Stat3 activating cytokines/cytokine receptor/JAKs/TYK2 complex (JAK2_JAK1_JAK3-TYK2) → Cytokine receptor/JAKs/TYK2 complex (TYK2-JAK2_JAK1_JAK3) (modification, collaborate)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Wery-Zennaro et al., FEBS Lett 1999 : In keratinocytes, IL-4 induced JAK1 and JAK2 phosphorylation but, unlike in immune cells, IL-4 did not involve JAK3 activation for its signaling
Levine et al., Hematology / the Education Program of the American Society of Hematology. American Society of Hematology. Education Program 2006 (Myeloproliferative Disorders) : Activation of JAK-STAT signaling by JAK2V617F in some, but not all MPD patients with ET and MF led to the identification of the constitutively active MPLW515L allele in ET and MF
Lee et al., Int J Biochem Cell Biol 2007 (MAP Kinase Signaling System) : The OSM stimulated expression of SDF-1 in hATSCs was completely abrogated by pretreatment of the cells with U0126, an MEK-specific inhibitor, but not with AG490, a JAK2 inhibitor, or WHI-P131, a JAK3 inhibitor , suggesting that ERK, but not JAK2 and JAK3, is involved in the OSM induced expression of SDF-1
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
Lipka et al., Mol Cancer Ther 2008 (Myeloproliferative Disorders) : In line with these data, combination treatment using LS104 plus an ATP-competitive JAK2 inhibitor ( JAK inhibitor I ) led to synergistically increased apoptosis in JAK2V617F positive cells
Elliott et al., Haematologica 2009 (Myeloproliferative Disorders) : JAK kinase inhibitors, which effectively inhibited the proliferation of cells expressing V617F or K539L, also caused a dose dependent reduction in both mutant JAK2 and SOCS3 tyrosine phosphorylation
Marty et al., J Biol Chem 2009 (Neoplasms, Experimental...) : These data establish that MPL ( W515L ) with appended JAK2 matures through the ER/Golgi system in an inactive conformation and suggest that the MPL ( W515L ) /JAK2 complex requires membrane localization for JAK2 phosphorylation, resulting in autonomous receptor signaling
Byfield et al., Invest Ophthalmol Vis Sci 2009 (Disease Models, Animal...) : Inhibition of JAK with AG490 significantly reduced phosphorylated JAK2 ( P < 0.001 ), phosphorylated STAT3 ( P = 0.002 ), and IVNV area ( P = 0.033 ) in the 50/10 OIR+SO model compared with control
Kim et al., Molecular cancer 2010 : In addition, treatment of 32D/IL-2Rbeta cells with the compound led to a block in IL-2 dependent activation of JAK3/STAT5 but not IL-3 dependent activation of JAK2/STAT5
Medves et al., Haematologica 2011 (Myeloproliferative Disorders) : Although platelet derived growth factor receptors are capable of activating JAK2, KANK1-PDGFRß did not induce JAK2 phosphorylation in hematopoietic cells and a JAK inhibitor did not affect KANK1-PDGFRß induced cell growth
McFarland et al., Mol Cancer Ther 2011 (Brain Neoplasms...) : In these xenograft tumors, JAK2 and STAT-3 are constitutively active, but levels vary among tumors, which is consistent with the heterogeneity of GBMs. AZD1480 inhibits constitutive and stimulus induced phosphorylation of JAK2 and STAT-3 in these GBM xenograft tumors in vitro, downstream gene expression, and inhibits cell proliferation
Zhang et al., Diabetes 2012 (Diabetes Mellitus, Type 2...) : Moreover, JAK2/STAT3 is activated by Aß, and inhibition of JAK2/STAT3 signaling attenuates Aß-induced upregulation of SOCS-1 and insulin resistance in hepatocytes
Oakes et al., Immunity 1996 (Severe Combined Immunodeficiency) : Although IL-2 induced phosphorylation of IL-2R beta, JAK1 , and STAT5 all required the presence of JAK3 , IL-4 mediated phosphorylation of JAK1, STAT6, and insulin receptor substrates 1 and 2 did not