Ask about this productRelated genes to: NFATc1 antibody
- 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
Related articles to: NFATc1 antibody
- Periodontal regeneration remains challenging because conventional therapy does not predictably restore lost periodontal tissues. This study compared the periodontal remodeling responses associated with locally administered denosumab (DNS) and recombinant human growth hormone (rhGH) in experimental periodontitis. - Source: PubMed
Publication date: 2026/08/20
Saad Fatma AdelEl-Korashy Sabry AHamed Ahmed ARobaian AliHassanein Fatma E A - Liuwei Dihuang Wan (LWDHW), a classic traditional Chinese medicine formula, is widely used to treat various diseases associated with kidney deficiency and has shown satisfactory clinical efficacy in postmenopausal osteoporosis (PMOP). However, its pharmacological mechanisms remain unclear. To address this, we first analyzed the chemical components of LWDHW using LC-MS/MS, which identified 1,615 components. Network pharmacology then predicted that inflammation and the NF-κB signaling pathway are potential therapeutic mechanisms underlying LWDHW's effects on PMOP. Subsequently, 27 female C57BL/6J mice were randomly assigned to the Sham, Model, and LWDHW groups. Mice in the latter two groups underwent bilateral ovariectomy (OVX), and those in the LWDHW group received oral LWDHW at 9.75 g/kg/day for 8 weeks. Serum and femur samples were collected for Enzyme-Linked Immunosorbent Assay (ELISA), Micro-Computed Tomography (µCT), histological examination, and immunohistochemistry (IHC). Primary bone marrow-derived macrophages (BMMs) were treated with LWDHW and then subjected to TRAP staining and qRT-PCR. In OVX mice, LWDHW significantly alleviated bone loss and deterioration of bone microarchitecture, accompanied by reduced serum β‑CTX levels and decreased osteoclast numbers in femoral tissues. IHC staining revealed notably lower expression of TNF-α, IL-1β, and p-P65 in femoral tissues of LWDHW-treated mice compared to the model group. In vitro, TRAP staining demonstrated that LWDHW inhibited RANKL/M-CSF-induced osteoclast differentiation of BMMs and downregulated the expression of Ctsk, MMP9, and Nfatc1. Western blot analysis further showed that protein levels of P65, p-P65, IκBα, and p-IκBα were significantly decreased in BMMs following LWDHW treatment. Collectively, LWDHW alleviates postmenopausal osteoporosis, possibly by suppressing NF-κB signaling‑mediated osteoclastogenesis. - Source: PubMed
Publication date: 2026/07/28
Fu DanqingLi ShengzhouLi BangshuWang XuchengZhao Jian - The development of novel therapies for osteoporosis has attracted increasing attention. Rab27A is upregulated during osteoclast differentiation, and N6-methyladenosine (m6A) modification has emerged as an important epigenetic regulator in orthopedic diseases. Bioinformatic analyses predicted that Rab27A contains multiple m6A modification sites and interacts with several m6A-associated proteins. Knockdown experiments were performed to evaluate the role of Rab27A in osteoclast differentiation and osteoporosis using an ovariectomized (OVX) mouse model. Rab27A depletion attenuated osteoporosis and increased the bone formation percentage from 14.73% to 28.13% (P < 0.05) in OVX mice. Western blotting and quantitative PCR demonstrated that Rab27A knockdown reduced the protein and mRNA expression of the osteoclast markers TRAP, NFATc1, and c-FOS, thereby suppressing osteoclast differentiation of bone marrow-derived macrophages (BMMs) induced by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-κB ligand (RANKL). TRAP staining further showed that Rab27A depletion significantly reduced TRAP activity from 24.1% to 12.9% (P < 0.01) following M-CSF and RANKL induction. RNA immunoprecipitation assays confirmed interactions between Rab27A and the m6A reader proteins YTHDC1 and IGF2BP2. Nuclear and cytoplasmic fractionation demonstrated that YTHDC1 facilitates the cytoplasmic export of m6A-modified Rab27A. In addition, q-PCR and western blot analyses showed that knockdown of either YTHDC1 or IGF2BP2 reduced Rab27A expression and decreased the expression of TRAP, NFATc1, and c-FOS, thereby suppressing osteoclast differentiation induced by M-CSF and RANKL. Collectively, these findings indicate that YTHDC1-mediated cytoplasmic export and IGF2BP2-mediated stabilization of m6A-modified Rab27A promote osteoclast differentiation and contribute to bone loss in the OVX mouse model. - Source: PubMed
Publication date: 2026/08/11
Tang LianChen TaoYuan LinLiu YanshiJiang LujunWang ZiLiu BinLi Zhong - Endocardial cushions, derived from the atrioventricular canal (AVC) and outflow tract (OFT), serve as the primordia for the formation of the septum and valves. Improper morphogenesis of the endocardial cushion leads to septal and valvular abnormalities, which contribute to the largest proportion of congenital heart diseases (CHDs). The development and maturation of the endocardial cushion rely on endothelial-to-mesenchymal transition (EndMT), a process by which endocardial cells undergo morphological remodeling and develop into the endocardial cushion mesenchyme. This biological event is strictly governed by regional signals originating from the myocardium, endocardium, and mesenchyme. Various signaling pathways, including TGFβ/BMP, Wnt, Notch, Hippo/YAP, PI3K/AKT, VEGF, and mechanical stress, are involved in the modulation of endocardial cell proliferation, migration, and mesenchymal transition. Transcription factors, such as SMAD, SNAIL, TWIST, TBX2, SOX9, KLF2/4, and NFATc1, exert distinct effects on endocardial EndMT. Maternal environmental exposures can disrupt signaling pathways and transcriptional network during endocardial cushion development, thereby enhancing susceptibility to CHDs. This review summarizes the mechanistic pathways and transcriptional regulation in AVC endocardial cushion development and EndMT, highlighting their association with CHDs. - Source: PubMed
Publication date: 2026/08/07
Wang JinyuZhang WanyiJiang SiyingWang ZaoLi YanmingLi Tao - Phytoestrogens derived from natural products have emerged as potential alternatives to hormone replacement therapy (HRT) for alleviating menopausal symptoms with reduced adverse effects. However, the therapeutic potential and mechanistic basis of flaxseed-derived lignan secoisolariciresinol diglucoside polymer (SDGP) remain largely unexplored. This study aimed to investigate the synergistic effects of SDGP and a linusorb mixture (LOMIX) on menopausal symptoms and to elucidate their underlying molecular mechanisms. Estrogen receptor (ER) activation was evaluated using ERE-luciferase reporter assays and Western blot analysis in MCF-7 cells. Anti-osteoclastogenic effects were assessed in RANKL-induced RAW264.7 cells. An ovariectomized (OVX) rat model was used to examine efficacy on reproductive tissues and bone metabolism. Co-treatment with SDGP and LOMIX synergistically enhanced ER[Formula: see text]/ER[Formula: see text] phosphorylation and Akt activation, leading to increased transcription of ER target genes. The combination also suppressed osteoclast differentiation by inhibiting NF-[Formula: see text]B and MAPK signaling pathways, including c-Fos and NFATc1. In OVX rats, oral administration of the mixture restored vaginal cornification and uterine morphology, and significantly improved trabecular bone structure and bone mineral density. Notably, these effects were achieved without significant alterations in circulating estrogen, FSH, or LH levels. The combination of SDGP and LOMIX alleviates menopausal symptoms through non-hormonal activation of ER signaling and inhibition of osteoclastogenesis. These findings suggest a promising phytotherapeutic strategy for managing postmenopausal disorders with reduced risk of hormone-related side effects. - Source: PubMed
Publication date: 2026/08/12
Jang Won YoungYoon Ji HyeLee Seul BiLee Sung-JinShim Youn YoungReaney Martin J TYoo Byong ChulLee JongsungCho Jae Youl