◀ Back to IL4

IL4 — SOCS3

Text-mined interactions from Literome

Jackson et al., J Immunol 2004 : SOCS1 is primarily induced by IL-4 through a STAT1 dependent mechanism, whereas SOCS3 is induced mainly by GM-CSF
Yu et al., J Immunol 2004 : Surprisingly, IL-4 is a potent inducer of STAT1 activation in Th2 but not Th1 cells, and SOCS1 or SOCS3 expression is dramatically reduced in STAT1 ( -/- ) Th2 cells
Hebenstreit et al., Mol Immunol 2005 : SOCS-1 and SOCS-3 inhibit IL-4 and IL-13 induced activation of Eotaxin-3/CCL26 gene expression in HEK293 cells
Canfield et al., J Immunol 2005 : In murine splenic B cells, the suppressor of cytokine signaling (SOCS)3 is inducible by IL-4 via a mechanism independent of STAT6 and PI3K ... However, the IL-4 induction of SOCS3 is blocked by inhibitors of either the JNK or p38 MAPK pathways ( SP600125 and SB203580, respectively )
Dickensheets et al., Genes Immun 2007 : Unlike their common ability to induce expression of SOCS-1, IL-4 also induced expression of SOCS-2 but not SOCS-3 in macrophages, whereas IFN-gamma induced expression of SOCS-3 but not SOCS-2
Ratthé et al., J Leukoc Biol 2007 : It is interesting that IL-4 increased expression of SOCS3 at the mRNA and protein levels ... The effect of IL-4 on SOCS3 protein expression was increased markedly when the proteasome inhibitor MG132 was added to the cultures, but this was inhibited by cycloheximide, suggesting that SOCS3 is de novo synthesized in response to IL-4
Uchida et al., Eur J Immunol 2007 : Inhibition of SOCS3 by RNA interference up-regulated the phosphorylation of STAT3 and suppressed in vitro IL-4 production by IL-18 primed liver MNC stimulated with alpha-GalCer, but it did not affect IFN-gamma production
Albanesi et al., J Immunol 2007 : We further demonstrate that IL-4 and IL-13 activate STAT-6 and induce the suppressors of cytokine signaling (SOCS)-1 and -3
Ratthé et al., Br J Haematol 2008 (Cell Transformation, Neoplastic...) : Investigation of the interleukin (IL)-4/IL-4 receptor system in promyelocytic leukaemia PLB-985 cells during differentiation toward neutrophil-like phenotype : mechanism involved in IL-4 induced SOCS3 protein expression ... Utilization of catalase, cycloheximide and genistein inhibitors showed that IL-4 induced SOCS3 by a mechanism dependent on a complete NADPH oxidase complex, protein synthesis and tyrosine phosphorylation, but independent of production of reactive oxygen species
Kleinsteuber et al., Blood 2012 (Tuberculosis) : SOCS3 promotes interleukin-17 expression of human T cells
Romain et al., Arterioscler Thromb Vasc Biol 2013 (Aortic Aneurysm, Abdominal...) : Overexpression of SOCS3 in T lymphocytes leads to impaired interleukin-17 production and severe aortic aneurysm formation in mice -- brief report
Park et al., J Allergy Clin Immunol 2013 (Nasal Polyps...) : Nasal epithelial cell culture was used to elucidate the effect of IL-4 , IL-5, IL-6, IL-10, IL-13, IFN-?, TNF-a, and TGF-ß1 on SOCS1 and SOCS3 expression in sinus mucosa ... SOCS1 was induced by IL-4 , IL-13, IFN-?, and TNF-a, while SOCS3 expression was upregulated by IL-6, IL-13, IFN-?, and TNF-a