In this study, we postulated that IL-6, by up-regulating CASR expression in parathyroid, thyroid C-cell, and kidney tubule, reducing PTH secretion and renal calcium reabsorption, and increasing calcitonin secretion, contributes to altered calcium homeostasis.

Electrophoretic mobility shift and supershift assays revealed binding of Sp1 and Sp3 to the −88/−50 element upon IL-6 stimulation. Interestingly, preincubation with STAT3 antibody prevented the binding of Sp1 and Sp3 to the −88/−50 element, indicating that STAT3 is involved in IL-6-driven Sp1/Sp3 protein-DNA complex formation.

2024年7月24日 · Mechanistically, nuclear FAK was found to regulate SP1/IL-6-mediated T cell exhaustion and the transcription of proinflammatory cytokines/chemokines. These findings underscore FAK’s pivotal role in CD8 + T cell exhaustion within the immunosuppressive tumor microenvironment, suggesting that FAK is a promising target for advancing cancer ...

The functional cis-regulatory elements in the human IL-6 gene 5′ flanking region are found binding sites for NF-κB, specificity protein 1 (SP1), nuclear factor IL-6 (NF-IL-6) (also known as CAAT/enhancer-binding protein β), activator protein 1 (AP-1), and interferon regulatory factor 1 (Libermann and Baltimore 1990; Akira and Kishimoto 1992 ...

Here, we show that Ahr also negatively regulates production of the pro-inflammatory cytokine IL-6 by suppressing histamine production in macrophages stimulated by LPS. We found that Ahr-Sp1 complex, independent of Stat1, represses histidine decarboxylase expression by inhibiting LPS-induced Sp1 phosphorylation on Ser residues in macrophages ...

Upregulation of NRROS on the hydrogen peroxide (H 2 O 2)-mediated ROS generation and interleukin 6 (IL-6) secretion was measured. 15d-PGJ 2-induced NRROS expression was mediated through PI3K/Akt-dependent activation of Sp1 and FoxO1 and established the essential promoter regions.

2008年2月22日 · Our study shows that IL-6, sIL-6R, or both inhibit type II collagen production by rabbit articular chondrocytes through a transcriptional control. The cytokine and/or sIL-6R repress COL2A1 transcription by a -63/-35 sequence that binds Sp1.Sp3.

IL-6是在感染和组织损伤时迅速和短暂地产生的，通过刺激急性时相反应、造血和免疫反应来促进宿主防御。 天然免疫系统细胞在 Toll样受体 刺激下分泌IL-6，激活更多的免疫反应。 内皮细胞和平滑肌细胞在IL-6刺激下释放趋化因子，募集更多的免疫细胞。 B细胞在IL-6的影响下被刺激。 肝脏中的肝细胞在IL-6刺激下合成和分泌急性时相蛋白。 IL-6在T辅助细胞的分化中起着关键作用。 在肥胖患者中，脂肪细胞分泌的IL-6会出现系统性升高，导致肥胖表现出一种慢性炎症状态。 IL …

2024年7月24日 · Mechanistically, nuclear FAK was found to regulate SP1/IL-6-mediated T cell exhaustion and the transcription of proinflammatory cytokines/chemokines.

Mechanistically, nuclear FAK was found to regulate SP1/IL-6-mediated T cell exhaustion and the transcription of proinflammatory cytokines/chemokines. These findings underscore FAK's pivotal role in CD8+ T cell exhaustion within the immunosuppressive tumor microenvironment, suggesting that FAK is a promising target for advancing cancer ...