Gene interactions and pathways from curated databases and text-mining

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IL4 — JAK2

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
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