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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to IL4

IL4 — JAK3

Pathways - manually collected, often from reviews:

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
Haque et al., J Biol Chem 2000 : We show that the SH2 domains of SOCS-2, SOCS-3, and cytokine-inducible SH2 containing protein are functionally redundant in regulating the IL-4 dependent Jak-Stat signaling ... Thus, the Thr-Phe motif in the Pre-SH2 domain plays a critical role in SOCS-3 mediated inhibition of the IL-4 dependent Jak-Stat signaling, likely by regulating the mode of SOCS-Jak interaction
Suzuki et al., Blood 2000 : These results indicate that gamma(c)- and Jak3 dependent signaling is essential for IL-4- and IL-9 induced proliferation and survival of murine mast cells, that the effects of IL-4 are mediated by type I IL-4R and that type II IL-4R is absent on mast cells, and that IL-4 phosphorylates the 65-kd isoform of Stat6 in mast cells in a gamma(c)- and Jak3 dependent manner
Doucet et al., Oncogene 2000 (Lung Neoplasms...) : In addition to these pathways, in lung tumor myofibroblasts, IL-4 and IL-13 induced the phosphorylation of JAK3 and increased the phosphorylation of Tyk2
Day et al., Oncogene 2002 : Our results suggest that the IL-4 and HGF pathways converge at multiple levels, and that IL-4 dependent Jak3 and STAT6 activities modulate signaling events independent of PI3K to enhance HGF dependent mitogenesis in myeloid cells, and possibly other common cellular targets
Doucet et al., Eur J Immunol 2002 (Inflammation) : Here we show that in normal lung fibroblasts IL-4 and IL-13 induce the expression of the gamma c chain and its association with Janus kinase (JAK) 3 , while lung myofibroblasts constitutively express a gamma c chain displaying a limited association with JAK3
Lutz et al., J Immunol 2002 : The IL-4R signaling for DC maturation requires the IL-4R alpha-chain and STAT6, but not Janus kinase 3 , indicating that IL-4R type II signaling is preferentially responsible for these effects
Zhou et al., J Immunol 2003 : Thus, in humans, IL-4 alone is sufficient to drive AID expression, and CD40 signaling is required for optimal AID production ; IL-4 induced AID expression is mediated via the JAK/STAT signaling pathway, and can be negatively regulated by the JAK phosphatase activity of CD45
To et al., Br J Cancer 2004 (Cell Transformation, Neoplastic...) : The interleukin mediated Janus kinase ( JAK ) /STAT pathway plays a crucial role in carcinogenesis
Yamashita et al., FEBS Lett 2010 : We found that flavones inhibited IL-4 induced epsilon germline transcription which is essential for IgE class switching, and the phosphorylation of signal transducer and activator of transcription 6, janus kinase 3 , and IL-4Ralpha, whereas IL-4 signaling mediated through type II IL-4R was unaffected by flavones
Horio et al., Naunyn Schmiedebergs Arch Pharmacol 2010 : IL-4 activated STAT6 ( signal transducer and activator of transcription 6 ) in HeLa cells, and up-regulation of H1R mRNA and activation of STAT6 by IL-4 were inhibited by a specific JAK3 ( Janus activated kinase 3 ) inhibitor
Heller et al., J Biol Chem 2012 : Our data suggest that a smaller ( 5 amino acid ) interval than previously determined is necessary for JAK3 activation/?C mediated signaling in response to IL-4 and IL-2
Keegan et al., Proc Natl Acad Sci U S A 1995 : Interestingly, although IL-4 induced the tyrosine phosphorylation of JAK3 , we did not detect JAK3 phosphorylation in response to IL-13
Tortolani et al., J Immunol 1995 (Leukemia) : In addition, IL-4 and IL-7 induced the rapid tyrosine phosphorylation of JAK3 and JAK1, and IL-4 activated both JAK3 and JAK1 phosphotransferase activity
Fenghao et al., J Clin Invest 1995 : Congruous with the involvement of a Stat protein, IL-4 induced robust Janus kinase 3 (JAK3) activity in BL-2 cells ... These results show that IL-4 NAF is IL-4 Stat, which is activated by JAK3 in response to IL-4 receptor engagement
Malabarba et al., J Biol Chem 1995 : Indeed, when human IL4R alpha was stably expressed in mouse BA/F3 cells, robust IL4 induced proliferation and JAK3 activation occurred without detectable involvement of JAK1, JAK2, or TYK2
Brunn et al., J Biol Chem 1995 : Both IL-2 and IL-4 stimulated the rapid activation of JAK1 and JAK3 , whereas JAK2 activity was unaffected by either cytokine
Welham et al., J Biol Chem 1995 (Leukemia, Erythroblastic, Acute...) : IL-4 also activated the Jak-3-kinase , but, despite other similarities, IL-13 did not
Russell et al., Science 1994 (Severe Combined Immunodeficiency) : IL-2, IL-4 , IL-7 ( whose receptors are known to contain gamma c ), and IL-9 ( whose receptor is shown here to contain gamma c ) induced the tyrosine phosphorylation and activation of the Janus family tyrosine kinases Jak1 and Jak3
Witthuhn et al., Nature 1994 : Here we describe a new Jak family kinase, Jak-3, and demonstrate that Jak-3, and to a lesser extent Jak-1, are tyrosine phosphorylated and Jak-3 is activated in the responses to interleukin-2 and interleukin-4 in T cells and myeloid cells
Murata et al., J Immunol 1996 (Colonic Neoplasms) : IL-4 also stimulated all three kinases and substrates, but unlike in immune cells, IL-4 did not involve JAK3 activation for its signaling in colon cancer cell lines
Chuang et al., J Biochem 1996 (Carcinoma, Hepatocellular) : Interleukin 4 , but not insulin, stimulated the tyrosine phosphorylation of JAK1 and, to a lesser extent, JAK2
Wang et al., J Immunol 1997 (Fibrosarcoma) : It has been shown that IL-4 induces the tyrosine phosphorylation of JAK1 and JAK3 in the majority of hemopoietic cell types, and JAK2 and TYK2 in several other types
Taylor et al., J Biol Chem 1997 (Severe Combined Immunodeficiency) : We found that although IL-4 stimulation of X-SCID B cells did not result in Janus tyrosine kinase-3 (JAK3) phosphorylation, other IL-4 substrates including JAK1 and IRS-1 were phosphorylated
Chuang et al., Biochem Biophys Res Commun 1997 (Carcinoma, Hepatocellular) : In contrast, IL-4 stimulated tyrosine phosphorylation of JAK1, JAK2 and tyk2 in this cell line
Candotti et al., Blood 1997 (Severe Combined Immunodeficiency) : Abnormalities in tyrosine phosphorylation of JAK3 in response to interleukin-2 (IL-2) and IL-4 were present in all patients
Siemasko et al., J Immunol 1998 : The signal transduction pathway utilized by IL-4 to induce IgG1 involves tyrosine phosphorylation of the IL-4 receptor, JAK1 , JAK3, and STAT6 proteins induced by IL-4 binding to the IL-4R
Harada et al., Biochem Biophys Res Commun 1998 : Interleukin-4 (IL-4) has been shown to activate Janus kinase (Jak)-1 and Jak-3 , followed by activation of STAT ( signal transducers and activators of transcription ) 6
Matsumoto et al., J Immunol 1999 (Dermatitis, Atopic...) : The stimulation with CD40L and/or IL-4 resulted in tyrosine phosphorylation of Janus kinase 3 (JAK3) in B cells, which was more strongly inducible in NC/Nga mice than in BALB/c mice