据报道,核因子kappa-B(NF-κB)信号可调控小胶质细胞的极化,而肿瘤坏死因子受体相关因子6(TRAF6)在此过程中可通过泛素化激活NF-κB通路。芳香烃受体(AHR)通过TRAF6参与调节NF-κB信号的激活点3。 有研究表明,慢性炎症和神经退行性病变贯穿CSVD的整个病理过程4。既往研究显示,C.EDA在缺血性卒中动物模型中可发挥抗炎...
Ovrevik J, Lag M, Lecureur V, Gilot D, Lagadic-Gossmann D, Refsnes M, Schwarze PE, Skuland T, Becher R, Holme JA (2014) AhR and Arnt differentially regulate NF-kappa B signaling and chemokine responses in human bronchial epithelial cells. Cell Commun Signal 12:1...
totic NF-kappa B pathway)J].Immunol,2002,169(6)：2846—2850.[17]Wu H,Jones R M,Neish A S.The Sahnon^lll effector AvrA mediates bacterial intracellular survival during infection ic vivo [J].Cell Microbiol,2012,14(1)：28—39.[18]Lu R,Wu S,Liu X,et al Chronic eXects of a Slhm...
ahr信号传递的替代途径也进行了描述,诸如结合至视网膜母细胞瘤蛋白,雌激素受体(er),转录因子e2f1和nfκb途径亚单元rela和relb。ahr也可作为泛素连接酶。因此,通过ahr的信号传递包含多种途径,包括组成型和非组成型ahr信号传递通路或信号传递活性,本文对这些术语进行了定义。 如本文所用,“组成型ahr信号传递”是指一...
(CREB-Binding Protein)/p300). In addition, AHR is also known to interact with signaling pathways that are mediated by ESR (Estrogen Receptor) and other Hormone receptors, Hypoxia, NF-KappaB (Nuclear Factor-Kappa-B) and Rb (Retinoblastoma) protein (Ref.1 2). Normally, AHR exists in a ...
Furthermore, S164 and its tryptophan metabolite, ILA, ameliorate intestinal barrier injury and suppress intestinal inflammation by activating the AhR-Nrf2 pathway and inhibiting the nuclear factor kappa-B (NF-kappa B) pathway. These results suggest that L. plantarum DPUL-S164 ameliorates intestinal ...
YS-1617B Anti-NF-κBp50(p50 NF-kappa B;p50NFKB) 细胞核因子50/κ基因结合核因子50抗体YS-1618B Anti-NGF-R/p75NTR/CD271(p75 Neurotrophin R) 神经生长因子受体抗体YS-1619B Anti-NGF-β 神经生长因子-β抗体YS-1620B anti-NGN3(neurogenin 3; Neurog3) 神经元素3抗体YS-1621B Anti-NGX6 (...
CS exposure also induces the overexpression of other inflammatory signaling pathways such as nuclear factor kappa B (NF-κB) and TNF-α [59]. It also reduces the expression of AhR protein in lung, decreasing the protective capacity of AhR against inflammatory and oxidative damages in lung [60]...
(nuclear factor kappa B,NF-κB)信号通路的持续性异常活化是导致AHR在HTLV-1阳性T细胞中恒定高表达的重要原因;(4)病毒蛋白Tax可以通过激活NF-κB来提高AHR的表达.以上的研究结果表明:NF-κB信号通路的持续性异常活化为AHR在HTLV-1阳性T细胞中的恒定高表达奠定了基础,这赋予了HTLV-1可以根据微环境中AHR配体的水平...
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