2022年2月25日 · HMGB1 also binds to toll like receptor 4 (TLR4) to inhibit nitric oxide synthase 3 (NOS3, also known as eNOS) expression and subsequent NO release in the setting of diabetes 76,77. These...

2023年9月21日 · 胞外HMGB1与 RAGE 、 TLR2 、 TLR4 等受体结合，激活 MyD88 从而导致NF-κB信号通路的激活进行信号传导，促进细胞因子 TNF 、 IL-6 、 IFN-γ 的产生和细胞存活。 HMGB1相关信号通路（源自参考文献） HMGB1通过两种方式释放到细胞外。 一种是HMGB1在细胞核内乙酰化后主动释放，另一种是细胞坏死过程中被动释放。 HMGB1从坏死细胞中释放或被激活的巨噬细胞分泌后，其功能是招募炎症细胞并在自然杀伤（NK）细胞、树突状细 …

2023年9月4日 · HMGB1 can interact with TLRs (TLR2, TLR4, and TLR9) to activate TLR signaling. Upon stimulation by the ligand, TLRs recruit downstream junction molecules, including TIR domain-containing adapter-inducing IFN-β (TRIF) and MyD88, which subsequently activate the NF-κB and IRF signaling pathways, promote the production of cytokines and chemokines ...

观察哮喘小鼠肺组织高迁移率族蛋白B1（HMGB1）、Toll样受体4（TLR4）和核因子κB（NF-κB）mRNA和蛋白表达变化，以及维生素D的干预作用。 将48只BALB/c小鼠随机分为对照组、哮喘组和1,25- (OH)2D3干预组，每组16只。 建立哮喘动物模型，干预组在每次雾化激发前给予腹腔注射1,25- (OH)2D3（4 μg/kg）。 分别在雾化激发1周和2周采集各组标本，常规苏木精-伊红（HE）染色测定气道壁厚度；免疫组化染色观察HMGB1、TLR4和NF-κB在肺组织中的表 …

2018年5月10日 · Our results demonstrate that: 1) intact HMGB1 binds to TLR4 via the A-box domain with high affinity but an appreciable dissociation rate; 2) intact HMGB1 binds to MD-2 via the B-box domain with low affinity but a very slow dissociation rate; and 3) HMGB1 A-box domain alone binds to TLR4 more stably than the intact protein and thereby ...

Here we demonstrate that in human whole blood, neutralizing antibodies against Toll-like receptor 4 (TLR4, but not TLR2 or receptor for advanced glycation end product) dose-dependently attenuate HMGB1-induced IL-8 release. Similarly, in primary human macrophages, HMGB1-induced TNF release is dose-dependently inhibited by anti-TLR4 antibodies.

2018年5月10日 · Recently, we demonstrated that: 1) the TLR4/MD-2 receptor is required for HMGB1-mediated cytokine production and 2) the HMGB1-TLR4/MD-2 interaction is controlled by the redox state of HMGB1 isoforms.

2024年5月9日 · hmgb1可以与tlr（tlr2、tlr4和tlr9）相互作用，激活tlr信号，在配体的刺激下，tlrs招募下游连接分子，包括含tir结构域的适配器诱导ifn-β（trif）和myd88，这些分子随后激活nf-κb和irf信号通路，促进参与免疫反应的细胞因子和趋化因子的产生，并诱导炎症。

6 天之前 · Results: HMGB1 expression increases after ischemic stroke and further affects the expression of TLR4, RAGE and other related inflammatory factors, thus reducing the inflammatory response and ultimately protecting against injury. These results confirmed the effect of HMGB1 on TLR4/RAGE signaling and the subsequent regulation of inflammation ...

2023年9月26日 · The interaction of HMGB1 with RAGE, TLR2, and TLR4 will transduce cellular signals that stimulate NF-κB and MAPK pathways, subsequently promoting the nuclear HMGB1 acetylation and secretion. JAK/STAT activation induces the translocation of HMGB1 from the nucleus towards the cytoplasm and its subsequent release into the extracellular space.