Ask about this productRelated genes to: NFATC3 antibody
- Gene:
- NFATC3 NIH gene
- Name:
- nuclear factor of activated T cells 3
- Previous symbol:
- -
- Synonyms:
- NFAT4, NFATX
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-16
- Date modifiied:
- 2017-12-06
Related products to: NFATC3 antibody
Related articles to: NFATC3 antibody
- Numerous cutaneous adnexal tumors have recently been characterized by specific molecular hallmarks, notably oncogenic gene fusions. Herein, we report three cases of a sweat gland tumor exhibiting a secretory morphology and harboring SFPQ::NFATC3 or NPM1::NFATC3 fusions. The cases presented in a 36-year-old woman (left thigh), a 55-year-old man (paraumbilical region), and a 65-year-old woman (scalp), and were dermal-based neoplasms. Histopathological examination revealed ill-defined tumors with an infiltrative growth pattern, predominantly centered in the dermis, with one case extending into the subcutis. Two cases were characterized by cords, small nodules, and nests of epithelioid cells with large hyperchromatic nuclei, while prominent glandular and cribriform structures were observed in the third case. Numerous round ductal structures filled with a dense eosinophilic secretory material were identified in all cases. Mitotic activity was very low (< 1/mm²). No lymphovascular or perineural invasion was observed. Immunohistochemistry demonstrated diffuse SOX10 positivity in one case and p63 expression in the remaining two. PanTRK and NUT were negative, and YAP1 expression was preserved. Molecular analysis revealed in-frame SFPQ::NFATC3 (n = 2) or NPM1::NFATC3 (n = 1) fusions with identical breakpoints within the NFATC3 gene. These three cases of sweat gland tumor harboring NFATC3 gene fusions may represent the first identified examples of a previously undescribed adnexal tumor. - Source: PubMed
Publication date: 2026/07/24
Kervarrec ThibaultCalonje EduardoPissaloux Danielde la Fouchardière ArnaudHaider ZahraOnuba LouisaLouveau BaptisteMourah SamiaTirode FranckBattistella MaximeMacagno Nicolas - Pinoresinol diglucoside (PDG), an active component derived from Eucommia ulmoides, exhibits therapeutic effects against apoptosis, inflammation, and hypertrophy, etc. However, whether PDG plays a protective role in diabetic cardiomyopathy (DCM) is not fully elucidated. This study aimed to investigate the role and potential mechanism of PDG in DCM. The possible mechanism of PDG targeting DCM was identified by network pharmacology, bioinformatics, machine learning and molecular docking methods. The heart function of mice was evaluated using echocardiography. The pathological changes in the heart of mice were detected using H&E staining. Changes of Ca fluorescence intensity values in H9c2 cells were assessed by confocal microscopy. Apoptosis was evaluated by TUNEL staining and flow cytometry. The expression of DCM-related genes and proteins, both in vivo and in vitro, was examined by qRT-PCR and Western blot. The results showed that PDG effectively improved the cardiac function and suppressed cardiac hypertrophy, inflammation, and cardiomyocyte apoptosis caused by DCM. Intriguingly, molecular docking results revealed that the therapeutic effect of PDG on DCM was associated with stromal interaction molecule 1 (STIM1), calcium release-activated calcium channel protein 1 (Orai1), and nuclear factor of activated T-cells 3 (NFAT3) signaling. Consistently, animal experiments results indicated that PDG significantly downregulated the expression of STIM1, Orai1, NFAT3 at the protein level, as well as the associated store-operated calcium entry (SOCE). Therefore, our findings revealed that PDG can alleviate cardiac hypertrophy, inflammation and apoptosis in DCM by downregulating the STIM1, Orai1, and NFAT3 signaling molecules. Thus, PDG may be a promising therapeutic candidate for treating DCM. - Source: PubMed
Feng YujieMao YananLi JunshuaiSun ZhipengWang YingchaoWang XinruWang FengLiu TiantianZhang Lane - Ventilator‑induced lung injury (VILI) is a serious complication of mechanical ventilation (MV). The mechanosensitive ion channel Piezo1 converts mechanical forces into biochemical signals; however, its specific role in the pathogenesis of VILI remains unclear. The present study aimed to investigate the role of Piezo1 in lung epithelial cells in mediating VILI and its downstream signalling mechanisms. To this end, the current study utilized a murine VILI model established by high tidal volume MV, lung epithelial‑specific knockout mice, and cyclic stretch of mouse lung epithelial (MLE‑12) cells combined with genetic knockdown or pharmacological inhibition of . Immunofluorescence and immunohistochemical analyses revealed that protein expression was significantly upregulated in the lung epithelium . Lung epithelial‑specific knockout mice exhibited markedly attenuated MV‑induced lung injury, barrier dysfunction and inflammatory responses. , cyclic mechanical stretch similarly upregulated Piezo1 expression in mouse lung epithelial MLE‑12 cells, accompanied by cytoskeletal disruption, and release of proinflammatory cytokines IL‑6, TNF‑α and IL‑1β, as assessed using ELISA. Genetic knockdown or pharmacological inhibition of effectively alleviated these injury phenotypes. Mechanistically, Piezo1 activation mediated stretch‑induced Ca influx, which triggered calcineurin activation and subsequent nuclear translocation of the transcription factor NFATc3, ultimately driving the release of proinflammatory cytokines, including IL‑6, TNF‑α and IL‑1β. In conclusion, the results of the present study revealed a novel Piezo1/Ca/calcineurin/NFATc3 signalling axis that drives pulmonary epithelial inflammation and barrier dysfunction in VILI, suggesting that Piezo1 and its downstream signalling molecules are potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/30
Li MinZhang Shu-LiYuan FengFeng Dan - Fabricating anisotropic multifunctional bioadhesive patches with tunable mechanical stiffness, conductivity, antimicrobial activity, and modulating cellular behavior is crucial for successfully managing cardiac tissue injury and boosting immunogenic microenvironments. Inspired by the native myocardium, we developed a 3D printable, anisotropic, and bioadhesive cardiac patch with tunable stiffness by incorporating conductive nanofillers (GO@ND) into a biocompatible hydrogel (CSA) for regulating cardiomyogenic cues. Incorporating GO@ND enhanced the conductivity with high interfacial toughness (>250 MJ m) and improved the printability with concentration-dependent self-assembly into the CSA matrix. Moreover, the electromechanical study revealed that CSA with higher stiffness (∼6.2 kPa) activated cytoplasmic YAPs during macrophage polarization and exhibited strong antibacterial efficacy. Besides, the stiffness and bioelectrical stimulation regulated human cardiomyocyte differentiation through anisotropic force-driven mechanosensors, triggering the phosphorylation of NFATc3 and activating Lamin A/C in a YAP-dependent manner. In the rat myocardial infraction (MI) model, the nanoengineered patch significantly reduced fibrosis, repaired the myocardium, and enhanced cardiac function. Based on these findings, we anticipated that the 3D-printed nanoengineered patch had tremendous potential for regulating the cardiac microenvironment with multifunctional abilities. - Source: PubMed
Publication date: 2026/04/02
Dutta Sayan DebAn Jeong ManPatil Tejal VKim HojinSantra Tuhin SubhraLee Yong-KyuLim Ki-Taek - Neural crest stem cells (NCSCs), capable of differentiating into neurons and Schwann cells, are essential for peripheral nerve regeneration. This study investigates the role of endogenous NCSC-like cells in mechano-electrical stimulation (MES)-enhanced peripheral nerve repair. In a critical-sized nerve injury model, MES leads to complete nerve reconnection, accompanied by a significant increase in NCSC-like cells at the injury sites. In vitro, MES promotes the simultaneous differentiation of NCSC-like cells into neurons and Schwann cells, with elevated neuregulin 1 (NRG1) expression, a key factor in Schwann cell development. Mechanistically, MES activates BMP/Smad signaling, driving neuronal differentiation and subsequent NRG1 secretion, which in turn promotes Schwann cell maturation through the ErBB/NFAT pathway. These findings demonstrate that MES enhances peripheral nerve regeneration by activating and directing stem cell differentiation, supporting a novel therapeutic approach that utilizes physical stimulation for stem cell modulation for nerve repair. - Source: PubMed
Publication date: 2026/03/26
Tai YouyiJin LuTonmoy Thamidul IslamPark B HyleNam Jin