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IL4 — STAT3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: STAT3 → IL4 (increases) Doucet et al., Oncogene 2000*
  Evidence: the constitutive phosphorylation of STAT3 was observed repeatedly in tumor myo®bro- blasts (Figure 6f), but only occasionally in normal ®broblasts (Figure 6e). In the latter cells, IL-4 and IL- 13 induced (Figure 6d) or increased (Figure 6e) the tyrosine phosphorylation of STAT3, whereas in tumor myo®broblasts the two cytokines only caused an increase in the phosphorylation of STAT3 (Figure 6f).

Text-mined interactions from Literome

O'Brien et al., J Biol Chem 1999 : STAT3 activation in stromal/osteoblastic cells is required for induction of the receptor activator of NF-kappaB ligand and stimulation of osteoclastogenesis by gp130 utilizing cytokines or interleukin-1 but not 1,25-dihydroxyvitamin D3 or parathyroid hormone
Wery-Zennaro et al., FEBS Lett 1999 : Furthermore, IL-4 stimulation of keratinocytes also induced tyrosine phosphorylation of STAT3 which was found to bind to the phosphorylated IL-13Ralpha(1)
Umeshita-Suyama et al., Int Immunol 2000 : Expression of IL-13R alpha 1 evoked STAT3 activation by IL-4 and IL-13, and in stimulated human B cells, on which IL-13R alpha 1 was highly expressed, IL-4 and IL-13 induced STAT3 activation
Prokopchuk et al., Br J Cancer 2005 (Pancreatic Neoplasms) : Interleukin-4 enhanced activity of MAPK, Akt-1, and Stat3 in IL-4-responsive, but not in IL-4-unresponsive MIA PaCa-2 cells ; however, IL-4 enhanced tyrosine phosphorylation of insulin receptor substrate-1 and -2 in all cell lines
Faffe et al., J Allergy Clin Immunol 2005 : The constitutively active form of STAT-3 increased eotaxin promoter activity, whereas the mutant form of STAT-3 that can not be phosphorylated significantly reduced eotaxin promoter activity induced by OSM or IL-4 plus OSM
Rahaman et al., Cancer Res 2005 (Glioblastoma) : Here, we show that IL-4 , which activates Stat6 in normal human astrocytes and in a variety of other cells, induces an aberrant activation of Stat3 in glioblastoma multiforme ( GBM ) cells but not in normal human astrocytes ... Now, we show that Stat3 is further activated by IL-4 stimulation of GBM cells ... In addition, transient expression of the IL-13Ralpha2 transgene in 293T cells increases the IL-4 mediated activation of Stat3 and subsequent expression of Stat3 targeted gene
Chiba et al., J Smooth Muscle Res 2009 (Asthma...) : In contrast, neither IL-13 nor IL-4 induced phosphorylation of STAT3
Pechkovsky et al., Clin Immunol 2010 (Idiopathic Pulmonary Fibrosis...) : IL-4/IL-10 stimulation induces a strong activation of STAT3 in AM from fibrosis patients
Ozawa et al., Journal of ophthalmology 2011 : In innate chorioretinal inflammation, interleukin-6 family ligands induce STAT3 activation in photoreceptors, which causes UPS mediated excessive degradation of the visual substance, rhodopsin
Choi et al., J Invest Dermatol 2013 (Hypopigmentation) : Despite the lack of a direct inhibition of melanin pigment synthesis, IFN? and IL-17A increased the synthesis of an antimelanogenic cytokine IL-6 in NHMs. IFN? activated signal transducers and activators of transcription 1 ( STAT1 ) and STAT3 phosphorylation in NHMs, and IL-4 increased the STAT3 and STAT6 phosphorylation
Murata et al., J Immunol 1996 (Colonic Neoplasms) : Both IL-13 and IL-4 induced phosphorylation of IL-4 STAT ( STAT6 ) but not STAT1, STAT3 , or STAT5