核因子受体激活因子-κB配体 (receptor activator for nuclear factor-κB ligand，RANKL)是由位于人染色体13q14上的基因Tnfsf11编码的可溶性蛋白，存在于OBs、T淋巴细胞、B淋巴细胞及骨髓间充质干细胞膜上，是骨代谢重要的调节分子。 骨髓中的髓系祖细胞可通过分化，产生不同形态结构、功能特征的细胞类群。 其主要由RANKL介导分化，得到的多个单核巨噬细胞再经相互融合可形成多核巨细胞即OCs。 OCs通过产生盐酸溶解骨中的矿物质，随后分泌金属蛋白酶，分解胶原 …

2012年12月14日 · These results demonstrate that reduction of CXCL16–CXCR6 is critical in RANKL-mediated osteoclastogenesis, which is mainly through the activation of JAK2/STAT3 signaling. CXCL16–CXCR6 axis may become a novel target for the therapeutic intervention of bone resorbing diseases such as rheumatoid arthritis and osteoporosis.

2022年10月1日 · Studies have shown that cytokines mainly promote the formation of OCs and play a role in bone resorption by stimulating OBs to express receptor activator of NF-κB ligand (RANKL). JAK/STAT plays a crucial role in the process of bone destruction. And JAK/STAT pathway mediates the RANKL/receptor activator of NF-κB (RANK)/osteoprotegerin (OPG) axis.

2017年7月14日 · Baricitinib suppressed 1,25D3 and PGE2-induced up-regulation of RANKL in osteoblasts, but not macrophage colony-stimulating factor expression. Moreover, the addition of recombinant RANKL to co-cultures completely rescued baricitinib-induced impairment of osteoclastogenesis. shRNA-mediated knockdown of Jak1 or Jak2 also suppressed RANKL ...

核因子-κB配体（RANKL）的受体激活剂是肿瘤坏死因子（TNF）家族的成员，在破骨细胞的分化和功能中起着至关重要的作用。 最近已显示趋化因子及其受体在破骨细胞形成中起关键作用，但是，CXCL16-CXCR6是否在RANKL介导的破骨细胞形成中起着未知的作用。

2013年2月13日 · This study investigated whether the calcineurin inhibitor, tacrolimus, suppresses receptor activator of NF-κB ligand (RANKL) expression in fibroblast-like synoviocytes (FLS) through regulation of IL-6/Janus activated kinase (JAK2)/signal transducer and activator of transcription-3 (STAT3) and suppressor of cytokine signaling (SOCS3) signaling.

In the current study, we demonstrate that a selective Jak1 and Jak2 inhibitor, baricitinib, inhibits osteoclastogenesis by suppressing RANKL expression in osteoblasts induced by 1,25D 3 and PGE 2 in vitro. Adenovirus-mediated knockdown of …

Studies have shown that cytokines mainly promote the formation of OCs and play a role in bone resorption by stimulating OBs to express receptor activator of NF-κB ligand (RANKL). JAK/STAT plays a crucial role in the process of bone destruction. And JAK/STAT pathway mediates the RANKL/receptor activator of NF-κB (RANK)/osteoprotegerin (OPG) axis.

This study was undertaken to investigate how selective inhibition of JAK with tofacitinib (CP-690,550) affects osteoclast-mediated bone resorption in a rat adjuvant-induced arthritis (AIA) model, as well as human T lymphocyte RANKL production …

目的 探讨JAK2/SATA3信号通路对核因子kB受体活化因子配体 (Receptor activator of NF-κB Ligand,RANKL)诱导RAW264.7细胞向破骨细胞分化过程的影响.方法 用ATP竞争性JAK2激酶抑制剂AG490与RANKL同时处理RAW264.7细胞,倒置显微镜观察细胞形态的变化,抗酒石酸酸性磷酸酶 (Tartrate-resistant ...