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
- The control of lymphatic permeability and flow is essential for homeostatic regulation of tissue fluid balance and immune responses. Histamine has been identified as an important signaling mediator involved in the regulation of lymphatic function. Histamine is released from activated perilymphatic mast cells and may also be produced by lymphatic endothelial cells (LECs) in response to flow-induced shear stress. The non-selective cation channel Transient Receptor Potential Vanilloid 4 (TRPV4) is an important mediator of signaling by GPCRs, including histamine receptors. TRPV4 is activated in response to shear stress and is functionally expressed by LECs. We hypothesized that histamine receptors and TRPV4 interact in LECs, leading to activation of distinct downstream signaling pathways. This study examined the mechanistic link between TRPV4 activity and histaminergic signaling in LECs. - Source: PubMed
Publication date: 2026/08/20
Retamal Jeffri SPeng ScottNguyen Thanh-NhanBandala-Sanchez EstherEriksson Emily MPokhrel RinaMcCague Roisin EMahdavian Narges SCarbone Simona ECao EnyuanGondin Arisbel BVeldhuis Nicholas APoole Daniel P - : Osteoarthritis (OA) is partly driven by an imbalance between bone-resorbing osteoclasts (OCs) and bone-forming osteoblasts (OBs). Collagen hydrolysates (CHs) are widely used for OA symptom management, with potential benefits attributed to bioactive peptides (BAPs) released during digestion. However, their direct effects on bone cells remain unclear. : Two bovine-sourced CHs, CH-GL and CH-OPT, were digested in vitro and tested on primary murine OC and OB cultures. Osteoclastogenesis was evaluated mainly under standard RANKL conditions (50 ng/mL), with exploratory analysis under high RANKL conditions (100 ng/mL). OC cultures were exposed to CH digesta at 0.01, 0.05, 0.1, or 0.5 mg/mL, while OB cultures were exposed to 0.01 or 0.1 mg/mL. : Under standard RANKL conditions, CH-GL significantly reduced OC area by over 50% across all tested concentrations, while OC number was not significantly altered. This coincided with decreased expression of selected osteoclastogenic markers, including , , , and . In OB cultures, CH-GL increased , , and expression at 0.1 mg/mL and reduced expression at both tested doses. It also modestly increased mineralization-related signal intensity and collagen-associated matrix area. For CH-OPT, selected reductions in and expression were observed, while OC number, OC area, and most OB-related outcomes were not significantly altered. : CH digesta modulated selected OC- and OB-related outcomes in primary murine cells. These preliminary in vitro findings support further investigation of CH-derived bioactives in models that more closely reproduce OA-associated joint pathology. - Source: PubMed
Publication date: 2026/08/18
Shan SiruiLarder Christina ETauer Josephine TIskandar Michèle MKomarova Svetlana VKubow Stan - Excessive osteoclast formation is a key contributor to pathological bone loss in disorders such as osteoporosis and rheumatoid arthritis. Asarinin, a natural lignan, has not previously been examined in the context of osteoclast differentiation. Here, we investigated the anti-osteoclastogenic effects of asarinin using RANKL-stimulated RAW264.7 cells. Asarinin significantly suppressed TRAP-positive multinucleated osteoclast formation. Mechanistically, asarinin selectively inhibited RANKL-induced phosphorylation of p38 and ERK MAPKs, leading to reduced c-Fos expression and inhibition of NFATc1 activation. In addition, asarinin disrupted actin ring formation in mature osteoclasts. Collectively, these findings identify asarinin as a pathway-selective inhibitor of osteoclast differentiation, acting through a mechanism consistent with modulation of the p38/ERK-c-Fos-NFATc1 signaling cascade while sparing parallel signaling pathways. - Source: PubMed
Publication date: 2026/08/11
Zhang LifangXie ChengxuBao XinyiLi XiaohanVelez HeribertoBasit FarwaDing YiliTabandeh MojtabaDeepak Vishwa - The long non-coding RNA is known to regulate various cellular processes; however, its role in porcine adipose tissue remains largely unexplored. In this study, we examined in pigs differing in fat-deposition traits by combining promoter sequencing, in silico analysis of transcription factor binding site analysis, expression profiling, and in vitro adipogenesis assays. We identified three novel polymorphisms in the promoter regions. Several SNPs were predicted to alter binding sites for transcription factors related to metabolism and immunity, such as , , and . One variant, rs329590882, differed significantly in frequency between breeds and may influence regulation. During adipocyte differentiation, expression of the isoform ENSSSCT00000080860 increased as adipogenesis progressed. Notably, this isoform was more highly expressed in lean-type Pietrain pigs than in the fatty Złotnicka Spotted (ZS) breed, suggesting that its function may not be directly related to fat accumulation. Additionally, we identified novel exon-exon junctions in , including a junction associated with the ENSSSCT00000077869 isoform. These findings provide new insights into the potential role of in porcine adipose tissue development and immunometabolic regulation and highlight the need for improved annotation of porcine lncRNAs. - Source: PubMed
Publication date: 2026/07/29
Piórkowska KatarzynaOcłoń EwaWróblewska KseniaZygmunt KarolinaPawlicki PiotrPardyak Laura - Osteoporosis (OP) is a chronic metabolic bone disease characterized by reduced bone mass, microarchitectural deterioration, and an increased risk of fragility fractures. Although conventional views have emphasized the imbalance between osteoblasts and osteoclasts, advances in osteoimmunology have shown that T-cell subsets regulate bone remodeling through multilayered mechanisms, including the RANKL/RANK/OPG axis, inflammatory cytokine networks, costimulatory molecules, immune checkpoints, the gut microbiota, and cellular metabolic reprogramming. Th17 cells and their signature cytokine IL-17 promote RANKL expression and amplify the NF-κB/MAPK/NFATc1 pathway of osteoclast differentiation, thereby constituting a key pathogenic component in inflammatory bone loss and postmenopausal osteoporosis. In contrast, regulatory T cells (Tregs) inhibit osteoclast formation through Foxp3-, IL-10-, TGF-β-, CTLA-4- and IDO-related pathways, thereby limiting proinflammatory T-cell activation and maintaining bone marrow immune homeostasis. Th1/Th2 cells, CD8+ T cells, γδ T cells, T follicular helper cells, NKT cells, and mucosa-associated unconventional T cells may also influence bone resorption and formation in different pathological contexts through factors such as IFN-γ, TNF-α, IL-4, IL-13, IL-21, IL-22, and membrane-bound RANKL. Drawing on the literature concerning T-cell subsets, the Th17/Tregs and Th1/Th2 balances, γδ T cells, and the RANKL/OPG axis, this review provides a narrative synthesis of current evidence about the molecular mechanisms by which T-cell subsets regulate osteoporosis-related bone remodeling, the features of immune imbalance in different types of osteoporosis, T-cell-targeted intervention strategies, and translational challenges. The aim is to provide a theoretical basis for developing precision antiosteoporotic therapies from an osteoimmune perspective. - Source: PubMed
Publication date: 2026/08/11
Gong YuanZeng WenxingLiao YitaoXie XuanyuQin ZhichaoLi ChaoZhang Xian