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首页> 外文期刊>Immunology Letters >Basic-helix-loop-helix transcription factor DEC2 constitutes negative feedback loop in IFN-beta-mediated inflammatory responses in human mesangial cells.
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Basic-helix-loop-helix transcription factor DEC2 constitutes negative feedback loop in IFN-beta-mediated inflammatory responses in human mesangial cells.

机译:碱性螺旋环螺旋转录因子DEC2构成人肾小球系膜细胞中IFN-β介导的炎症反应的负反馈环。

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摘要

Differentiated embryo-chondrocyte 2 (DEC2), a basic-helix-loop-helix transcriptional factor, is involved in various biological reactions by regulating the expression of its target genes. In the present study, we demonstrated DEC2 expression in response to the treatment with polyinosinic-polycytidylic acid (poly IC), an authentic double-stranded RNA, in cultured human mesangial cells. RNA interference against DEC2 enhanced the poly IC-induced expression of IFN-beta and its downstream genes, retinoic acid-inducible gene-I (RIG-I) and CCL5. Knockdown of TLR3 abolished the poly IC-induced DEC2 expression. DEC2 expression may constitute a negative feedback system for the IFN-beta/RIG-I/CCL5 pathway in the glomerulus, which may play a role in controlling protracted inflammatory reactions in the kidney.
机译:分化的胚胎-软骨细胞2(DEC2),一种基本的螺旋-环-螺旋转录因子,通过调节其靶基因的表达参与各种生物学反应。在本研究中,我们证明了在培养的人肾小球系膜细胞中,DEC2表达是对多肌苷-聚胞苷酸(poly IC)(一种真正的双链RNA)的反应。 RNA对DEC2的干扰增强了多聚IC诱导的IFN-β及其下游基因,维甲酸诱导基因I(RIG-1)和CCL5的表达。减少TLR3取消了多聚IC诱导的DEC2表达。 DEC2表达可能构成肾小球中IFN-β/ RIG-I / CCL5途径的负反馈系统,这可能在控制肾脏的长期炎症反应中起作用。

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