TGF-beta suppression of IFN-gamma-induced class II MHC gene expression does not involve inhibition of phosphorylation of JAK1, JAK2, or signal transducers and activators of transcription, or modification of IFN-gamma enhanced factor X expression.

作者: E. N. Benveniste , Yi-Ju Lee , R. B. Panek

DOI:

关键词: CD74Gene expressionBinding proteinTyrosine phosphorylationBiologyTranscription (biology)PhosphorylationTGF beta signaling pathwayMolecular biologyMessenger RNA

摘要: TGF-beta is a widely expressed immunoregulatory protein that exerts diverse range of effects on many types cells. One the inhibition both constitutive and cytokine-inducible class II MHC gene expression. In this study, we demonstrate inhibits expression surface protein, mRNA, promoter activity in primary astrocytes, dose time dependent. does not act to inhibit IFN-gamma-induced global fashion, as induction ICAM-1 IRF-1 by IFN-gamma unaffected treatment with TGF-beta. Furthermore, affect events are involved intracellular signaling such tyrosine phosphorylation JAK1, JAK2, STAT1 alpha, nor it X2 box binding enhanced factor X. We speculate may be exerting its modulating or function constitutively factors responsible for regulation astrocytes.

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