tlr4是类toll受体中主要的脂多糖(lps)受体，并且tlr4被lps激活。 MyD88-和TRIF-依赖的信号通路被连续触发，并偶联LPS激活的TLR4从质膜到胞内体重新分配。 TLR4在细胞内部的易位及其进一步的溶酶体降解促进了炎症反应的终止。

2025年2月6日 · TLR4（Toll样受体4）是模式识别受体（PRRs）家族的重要成员，在先天免疫系统中起着关键作用。 它能够识别病原体相关分子模式（PAMPs），如脂多糖（LPS）等，并触发炎症反应。

In RAW264.7 cells without LPS stimulation, baicalin dose-dependently inhibit the protein and mRNA expression of CD14, but not TLR4. In RAW264.7 cells with CD14 knockdown, baicalin pretreatment did not prevent inflammatory responses and activation of MyD88/NF-κB p65 pathway induced by high concentrations (1000 μg/mL) of LPS.

2024年12月30日 · TLR4（Toll样受体4）是Toll样受体家族中的重要成员，主要作为脂多糖（LPS）的受体，在识别并响应细菌等微生物成分的过程中发挥着关键作用。 当LPS与TLR4结合后，会触发一系列复杂的信号传导通路，这些通路对于启动和调控炎症反应至关重要。

Here, we further validated the contribution of the p65 and c-Rel subunits of NF-κB in transcriptionally inducing the Arid5a gene in the early phase of TLR4 stimulation. Our data suggest that IKK-mediated NF-κB signaling is the key regulator of Arid5a gene expression.

Our data reveal the temporal kinetics of pro- and anti-inflammatory signaling events that may be important therapeutic targets for inflammatory diseases. Keywords: Inflammation; TLR4; interleukin-10; lipopolysaccharide; nf-kappa B; tumor necrosis factor. Published 2018. This article is a U.S. Government work and is in the public domain in the USA.

The contents of p65 protein in myocardium and contents of p65,TLR4,i NOS and e NOS protein in thoracic aorta were detected by Western blot. As compared with NC group,the hemodynamic indexes in LPS group were significantly decreased; the contents of BNP,CK-MB and c Tn-Ⅰ in serum,TNF-α and IL-6 in plasma,p65 in myocardium,i NOS,e NOS,TLR4 and ...

2021年3月15日 · One of the downstream molecules of TLR4 is NF-κB, a heterodimer composed of p65 and p50 subunits, and nuclear translocation of NF-κB p65 is a sign of NF-κB activation. In the inactive state, the binding of NF-κB to the inhibitory protein IκB exists in an inactive form in the cytoplasm (Xia et al., 2006). After TLR4 was activated by LPS in ...

2024年12月20日 · Mechanistically, PRDX1-TLR4 signaling activates p65, promoting Saa3 and Acod1 expression while inhibiting Nfatc1, a master regulator of osteoclastogenesis. Remarkably, PRDX1 redirects p65 binding from Nfatc1 to Saa3 and Acod1 promoters, thereby suppressing osteoclast formation.

结果胆固醇肺炎泡沫细胞中TLR4蛋白阳性表达率、MyD88蛋白和NF-κB p65蛋白强阳性表达率明显高于对照组，差异有统计学意义 (P <0.05)。 TLR4阳性表达率、MyD88和NF-κB强阳性表达率均与性别不相关 (P >0.05)。 年龄<50岁者胆固醇肺炎泡沫细胞中TLR4阳性表达率、MyD88和NF-κB...