Title : SOCS3 transactivation by PPARγ prevents IL-17-driven cancer growth.

Pub. Date : 2013 Jun 15

PMID : 23619236






4 Functional Relationships(s)
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1 Activation of the transcription factor PPARgamma by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARgamma are incompletely characterized. Docosahexaenoic Acids peroxisome proliferator activated receptor gamma Mus musculus
2 Activation of the transcription factor PPARgamma by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARgamma are incompletely characterized. Docosahexaenoic Acids peroxisome proliferator activated receptor gamma Mus musculus
3 Activation of the transcription factor PPARgamma by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARgamma are incompletely characterized. Docosahexaenoic Acids peroxisome proliferator activated receptor gamma Mus musculus
4 Accordingly, TH17 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce interleukin (IL)-17 following activation of PPARgamma by DHA. Docosahexaenoic Acids peroxisome proliferator activated receptor gamma Mus musculus