◀ Back to JAK2
IL4 — JAK2
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
JAK2
→
IL4
(increases)
Doucet et al., Oncogene 2000*
Evidence: IL-4 and IL-13 also induced the tyrosine phosphorylation of JAK2 in both cell types (Figure 2e,f, upper blots) whereas JAK3 phosphorylation was detected only in lung myo®bro- blasts (Figure 2g,h, upper blots).
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NCI Pathway Database IL4-mediated signaling events:
IL4/IL4R/JAK1 complex (IL4-IL4R-JAK1)
→
IL4/IL4R/JAK1/IL13RA1/JAK2 complex (IL4-IL4R-JAK1-IL13RA1-JAK2)
(modification, collaborate)
Losman et al., J Immunol 1999, Haque et al., J Biol Chem 2000, Obiri et al., J Biol Chem 1995, Murata et al., J Immunol 1996, Obiri et al., J Immunol 1997, Miloux et al., FEBS Lett 1997
Evidence: mutant phenotype, assay, physical interaction
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NCI Pathway Database IL4-mediated signaling events:
IL4/IL4R/JAK1 complex (IL4-IL4R-JAK1)
→
IL13RA1/JAK2 complex (IL13RA1-JAK2)
(modification, collaborate)
Losman et al., J Immunol 1999, Haque et al., J Biol Chem 2000, Obiri et al., J Biol Chem 1995, Murata et al., J Immunol 1996, Obiri et al., J Immunol 1997, Miloux et al., FEBS Lett 1997
Evidence: mutant phenotype, assay, physical interaction
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NCI Pathway Database IL4-mediated signaling events:
SOCS1 (SOCS1)
→
IL4/IL4R/JAK1/IL13RA1/JAK2 complex (IL4-IL4R-JAK1-IL13RA1-JAK2)
(modification, inhibits)
Losman et al., J Immunol 1999, Haque et al., J Biol Chem 2000, Obiri et al., J Biol Chem 1995, Murata et al., J Immunol 1996, Obiri et al., J Immunol 1997, Miloux et al., FEBS Lett 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database IL4-mediated signaling events:
IL4/IL4R/JAK1/IL13RA1/JAK2 complex (IL4-IL4R-JAK1-IL13RA1-JAK2)
→
IL13RA1/JAK2 complex (IL13RA1-JAK2)
(modification, collaborate)
Losman et al., J Immunol 1999, Haque et al., J Biol Chem 2000, Obiri et al., J Biol Chem 1995, Murata et al., J Immunol 1996, Obiri et al., J Immunol 1997, Miloux et al., FEBS Lett 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database IL4-mediated signaling events:
IL4/IL4R/JAK1/IL13RA1/JAK2 complex (IL4-IL4R-JAK1-IL13RA1-JAK2)
→
STAT6 (STAT6)
(modification, activates)
Hou et al., Science 1994, Murata et al., J Immunol 1996
Evidence: mutant phenotype
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NCI Pathway Database IL12-mediated signaling events:
IL4 (IL4)
→
IL12Rbeta2/JAK2 complex (IL12RB2-JAK2)
(modification, inhibits)
Yamamoto et al., Biochem Biophys Res Commun 1999, Bacon et al., J Exp Med 1995, Hunter et al., J Immunol 1995, Presky et al., Proc Natl Acad Sci U S A 1996, Zou et al., J Biol Chem 1997, Gollob et al., Blood 1998
Evidence: mutant phenotype, assay, physical interaction, other species
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
Schnyder et al., J Recept Signal Transduct Res 2002
(Colorectal Neoplasms...) :
In the LS513 cells,
IL-4 stimulated phosphorylation of
Jak2 , an adapter molecule at the IL-4 receptor, and phosphorylation of transcription factor Stat6 both, in the absence and presence of IGF-1
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
Chen et al., J Biol Chem 2006
(Graves Disease) :
IL-4 activates
Jak2 in orbital fibroblasts
Ip et al., Clin Exp Immunol 2006
(MAP Kinase Signaling System) :
Inhibition of p38 MAPK, ERK and
JAK-2 activities by pretreating the cells with their corresponding inhibitors SB203580, PD98059 and AG490, respectively, significantly
suppressed IL-4- and IL-13 induced MCP-1 production in BEAS-2B cells
Ratthé et al., J Leukoc Biol 2007
:
We also demonstrated that
IL-4 induced phosphorylation of Syk, p38, Erk-1/2, JNK, Jak-1,
Jak-2 , STAT6, and STAT1 and that treatment of cells with the inhibitors piceatannol, SB203580, PD98059, or AG490 reversed the ability of IL-4 to delay neutrophil apoptosis
Choi et al., J Invest Dermatol 2013
(Hypopigmentation) :
In conclusion, the involvement of the
IL-4 induced
JAK2-STAT6 signaling and the IFN?- or IL-17A dependent antimelanogenic IL-6 production should be considered as one of the mechanisms explaining the association with hypopigmention in skin diseases
Murata et al., J Biol Chem 1995
(Colonic Neoplasms) :
The phosphorylation of JAK1 and
JAK2 was
induced by
IL-4 stimulation ; however, Tyk2 was constitutively phosphorylated, and IL-4 treatment further augmented this phosphorylation
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
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
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
Murata et al., Int Immunol 1998
:
The
Janus kinase (JAK)2 and Tyk2 were phosphorylated in
response to
IL-4 or IL-13 in sk559 and sk574 cell lines