NFAT4 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- NFAT4 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100543
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- NFAT4 antibody Polyclonal Antibodies Primary antibodies
Related genes to: NFAT4 antibody Polyclonal Antibodies Primary antibodies
- 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: NFAT4 antibody Polyclonal Antibodies Primary antibodies
Related articles to: NFAT4 antibody Polyclonal Antibodies Primary antibodies
- 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 - Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease characterized by autoimmune-mediated destruction of intrahepatic bile ducts. Emerging evidence suggests that circular RNAs (circRNAs) play regulatory roles in autoimmune diseases, but their involvement in PBC remains unclear. This study focused on the hsa_circ_0000711 and its potential mechanism in PBC pathogenesis. The study included 46 PBC patients, 40 healthy controls, and 40 patients with other liver diseases. Human intrahepatic biliary epithelial cells (HiBEpic) were treated with 1 mM glycochenodeoxycholic acid (GCDCA) to establish a PBC cell model. Hsa_circ_0000711 was overexpressed or knocked down using plasmid transfection and siRNA, respectively. Expression levels were analysed by qPCR/Western blot, cell viability by CCK-8, and hsa_circ_0000711-miR-185-5p interaction by luciferase assay. Serum hsa_circ_0000711 levels were significantly higher in PBC patients compared to healthy controls and other liver disease groups ( < 0.0001). GCDCA-treated HiBEpic cells showed increased expression of the E2 subunit of the pyruvate dehydrogenase complex (PDC-E2) and nuclear factor of activated T cells 3 (NFATc3), along with decreased cell viability. Overexpression of hsa_circ_0000711 increased PDC-E2 and NFATc3 expression and worsened cellular injury, while its knockdown reversed these effects. The dual luciferase assay confirmed that hsa_circ_0000711 directly binds to miR-185-5p, suppressing its activity and thereby relieving the repression of NFATc3. Hsa_circ_0000711 promotes PBC progression by sponging miR-185-5p and upregulating NFATc3, leading to bile duct epithelial cell injury. These findings highlight its potential as a novel diagnostic biomarker and therapeutic target for PBC. - Source: PubMed
Publication date: 2026/03/25
Lu WenlongLi WenshuaiWang PanCong PeishanWang ZhanGao WeizeSun GuirongLiu Mingjun - Ferroptosis, an iron-dependent form of programmed cell death driven by toxic lipid peroxide accumulation, plays a critical role in various diseases, making its modulation a promising therapeutic strategy. In this study, we identified defactinib, a specific inhibitor of FAK as a novel ferroptosis suppressors. We demonstrate that FAK/SRC-JNK signaling positively regulates ferroptosis by upregulating ACSL4, a critical mediator of ferroptosis. We reveal that a subset of JNK downstream transcription factors, including ATF2, NFATC1, NFATC3, and SMAD4, promote ferroptosis through direct binding to the ACSL4 promoter and activation of its expression. In contrast, another subset of JNK-associated transcription factors, including c-Jun, STAT3, ELK1, and HSF1, inhibit ferroptosis by binding to the ACSL4 promoter and repressing its expression. The net effect of FAK/SRC-JNK signaling in our models is a significant upregulation of ACSL4 and promotion of ferroptosis. Notably, elevated FAK/SRC-JNK signaling sensitizes cancer cells to ferroptosis-inducing therapies, while inhibition of the FAK/SRC-JNK signaling pathway protects against acute pancreatitis by suppressing ferroptosis. These findings highlight the central role of FAK/ SRC-JNK signaling in controlling ferroptotic cell death and underscore the therapeutic potential of targeting FAK/ SRC-JNK mediated ferroptosis, offering new avenues for the treatment of cancer and acute pancreatitis. - Source: PubMed
Publication date: 2026/03/20
Qin JianhuaMa ShuangWang JunyangHuang SiyuanLuan JingHe JiyuanHou GuoyuanSun NaZhang WeiGao Minghui - Extracellular vesicles (EVs) are increasingly recognized as critical mediators of intercellular communication, transferring a diverse repertoire of proteins, nucleic acids, and bioactive lipids that modulate the functional phenotype of recipient cells in both paracrine and endocrine manner. While the roles of EV-transported microRNAs (miRs) and proteins in pulmonary diseases have been extensively studied, the contribution of EV-encapsulated bioactive lipid mediators to the pathophysiology of pulmonary disorders, including acute respiratory distress syndrome (ARDS), remains largely underexplored. Here, we review the biosynthesis of bioactive lipids, their incorporation into EVs, and their roles in regulating pulmonary inflammation, injury, and resolution. We first highlight upstream signaling pathways, such as toll-like receptor 4 (TLR4) and the nuclear factor of activated T-cells cytoplasmic member 3 (NFATc3), which regulate the expression of lipid biosynthetic enzymes. We then examine how EV-encapsulated pro-inflammatory and pro-resolving lipids contribute to ARDS pathogenesis and clinical outcomes. Evidence supporting the role of EV-transported pro-resolving lipid mediators as key regulators of inflammation resolution and restoration of pulmonary homeostasis is also reviewed, along with their therapeutic potential in mitigating ARDS. Finally, we identify critical gaps in our understanding of how EV lipids modulate ARDS pathophysiology and discuss the challenges and opportunities for therapeutic targeting. - Source: PubMed
Publication date: 2026/02/11
Posham LalithyaWisler JonGowdy Kimberly MPei DehuaChristman John WKarpurapu Manjula