NFATC1 antibody - N-terminal region (P100981_P050)
- Known as:
- NFATC1 (anti-) - N-terminal region (P100981_P050)
- Catalog number:
- p100981_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NFATC1 antibody - N-terminal region (P100981_P050)
Related genes to: NFATC1 antibody - N-terminal region (P100981_P050)
- Gene:
- NFATC1 NIH gene
- Name:
- nuclear factor of activated T cells 1
- Previous symbol:
- -
- Synonyms:
- NF-ATC, NFATc, NFAT2
- Chromosome:
- 18q23
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-16
- Date modifiied:
- 2017-12-06
Related products to: NFATC1 antibody - N-terminal region (P100981_P050)
Related articles to: NFATC1 antibody - N-terminal region (P100981_P050)
- Osteoclast overactivation is a central driver of bone metabolic disorders such as osteoporosis, and novel drug targets for these diseases continue to be actively explored. Scaffold proteins, which enhance the specificity of deubiquitinase (DUB)-substrate interactions, have emerged as promising therapeutic targets for the sustained management of chronic diseases. Intraflagellar transport (IFT) proteins, recognized for their scaffolding roles in cellular signaling, are increasingly implicated in bone remodeling. However, their therapeutic potential for bone metabolic disorders remains to be fully elucidated. - Source: PubMed
Publication date: 2026/04/02
Gao YuanLai BowenYan RanHe JinnanLu TingweiYang ShiyuanChen JunGao RuiJiang HengZhou Xuhui - Pathological osteolysis, driven by excessive osteoclast activity, is a hallmark of Rheumatoid Arthritis (RA) and osteoporosis. Current therapies target inflammation but fail to prevent bone erosion, highlighting the demand for dual-action agents. Although Tripterygium wilfordii has shown therapeutic efficacy in RA, its clinical application is restricted by toxicity. Consequently, identifying novel bioactive monomers with favorable safety and deciphering their targets remains a critical need. - Source: PubMed
Publication date: 2026/04/15
Zhang XuanruiYang BiaoMa XiaoyuZhang WeijinXu XunpeiZhan HaoqinZhang ZhanrongZhou XuhuiZhang ZhengTao Zhengbo - The homeostatic balance of bone remodeling is governed by the precise coordination between bone-forming osteoblasts and bone-resorbing osteoclasts. In this study, we investigated the anti-resorptive properties of rhamnocitrin-3-rhamnoside (Rh3R), a flavonoid isolated from Loranthus tanakae, using primary bone marrow-derived macrophages (BMMs) and calvaria-derived osteogenic progenitor cells (COCs) to ensure biological relevance. Our findings demonstrate that Rh3R potently inhibits the RANKL-induced differentiation of BMMs into TRAP-positive multinucleated osteoclasts in a dose-dependent manner, without inducing cytotoxicity. Mechanistically, Rh3R effectively attenuates RANKL-induced downstream signaling cascades, as evidenced by the attenuated phosphorylation of MAPKs (ERK1/2, JNK, p38), AKT, and IκB. This signaling blockade subsequently suppresses the induction of the master transcription factors, c-Fos and NFATc1. Furthermore, Rh3R impairs the functional resorptive capacity of mature osteoclasts by destabilizing F-actin-rich ring structures accompanied by decreased integrin β3 expression, thereby preventing the formation of a functional sealing zone. The inhibitory effect of Rh3R on bone-degrading activity was further confirmed by a significant reduction in the total area of resorption pits on bone slices. Notably, Rh3R exhibits a lineage-specific inhibitory effect, showing no adverse influence on osteoblastogenesis or the mineralizing capacity of primary osteogenic cells. Furthermore, the effect of Rh3R was consistently maintained in a co-culture system of primary osteoblasts and BMMs. Collectively, these in vitro findings identify Rh3R as a bioactive modulator of osteoclast differentiation and function via suppression of RANKL-induced downstream signaling, warranting future in vivo and pharmacological studies to evaluate efficacy, exposure, and safety. - Source: PubMed
Yun Hyung-MunKim Soo HyunLee JoonyeopPark Kyung-Ran - Colitis and its associated bone loss are major global health concerns with limited therapeutic options. Portulaca oleracea L. polysaccharide (POP) has been suggested to ameliorate both conditions via microbiota modulation. The study aimed to explore whether POP can alleviate colitis-associated bone loss and its underling mechanism. - Source: PubMed
Publication date: 2026/04/13
Li KunZhu RuiqingChen YaboWang XunkangJiang YipingHan TingYue XiaoqiangXia TianshuangXin Hailiang - Postmenopausal osteoporosis (PMOP) represents the most prevalent metabolic bone disease among postmenopausal women worldwide. Cathepsin K (CTSK), a key mediator of osteoclastic bone resorption, serves as a critical therapeutic target for PMOP. Through structure-based virtual screening coupled with functional validation, we identified Tucatinib as a potent CTSK inhibitor. Microscale thermophoresis (MST), molecular docking, and CTSK activity assays confirmed that Tucatinib directly binds to and inhibits CTSK, effectively suppressing osteoclast-mediated bone resorption. Notably, Tucatinib attenuated NFATc1-driven osteoclast differentiation in bone marrow-derived monocytes/macrophages (BMMs). In ovariectomized mouse models, Tucatinib significantly prevented estrogen deficiency-induced bone loss. Mechanistic investigations revealed that Tucatinib maintains mitochondrial homeostasis by inhibiting dynamin-related protein 1 (DRP1) phosphorylation at Ser616 during early-stage osteoclast differentiation and reducing mitochondrial reactive oxygen species (mtROS) production, thereby stabilizing mitochondrial fission/fusion dynamics and suppressing NFATc1 activation. By simultaneously modulating of the DRP1/NFATc1 axis and CTSK enzymatic activity, offering a promising dual-action therapeutic strategy for PMOP. Our findings demonstrate that Tucatinib alleviates osteoporotic bone loss by simultaneously modulating the DRP1/NFATc1 axis and CTSK enzymatic activity, offering a promising dual-action therapeutic strategy for PMOP. - Source: PubMed
Publication date: 2026/04/11
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