NFATC2 _ NFAT1
- Known as:
- NFATC2 _ NFAT1
- Catalog number:
- Y214362
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- NFATC2 _ NFAT1
Related genes to: NFATC2 _ NFAT1
- Gene:
- NFATC2 NIH gene
- Name:
- nuclear factor of activated T cells 2
- Previous symbol:
- -
- Synonyms:
- NF-ATP, NFATp, NFAT1
- Chromosome:
- 20q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-16
- Date modifiied:
- 2017-12-06
Related products to: NFATC2 _ NFAT1
45 kDa NF-AT-interacting protein,45 kDa NFAT-interacting protein,Homo sapiens,Human,NFATC2-interacting protein,NFATC2IP,NIP45,Nuclear factor of activated T-cells, cytoplasmic 2-interacting protein45 kDa NF-AT-interacting protein,45 kDa NFAT-interacting protein,Mouse,Mus musculus,NFATC2-interacting protein,Nfatc2ip,Nip45,Nuclear factor of activated T-cells, cytoplasmic 2-interacting proteinanti-NFAT1anti-NFAT1anti-NFAT1 (2A4)anti-NFAT1 (2A4)anti-NFAT1 (2A4)anti-NFAT1 (2A4) type: Primary antibodies host: MouseAnti-NFAT1 Antibodyanti-NFAT1 type: Primary antibodies host: Mouseanti-NFATC2 (Internal)Anti-NFATc2 AntibodyAnti-NFATC2, Goat Polyclonal to NFATC2, Isotype , Host GoatAnti-phospho-NFAT1 (pSer54<_SUP>) produced in rabbit AntibodyAntibodies: NFATC2 _ NFAT1 HOST: Goat Clonality: pAb Related articles to: NFATC2 _ NFAT1
- As the only mammalian appendage capable of complete regeneration, deer antlers serve as an invaluable model to investigate cartilage regrowth, but the underlying mechanism remains unclear. This study revealed that addition of palmitic acid (PA), an abundant long-chain saturated free fatty acid, inhibited the proliferation and hypertrophy of antler chondrocytes while promoting chondrocyte apoptosis. PA treatment activated NOTCH1 signaling and restrained the transport of Ca from the cytosol to the endoplasmic reticulum (ER) via RBPJ (recombination signal-binding protein for immunoglobulin kappa J region)-targeted TMTC4 (transmembrane O-mannosyltransferase targeting cadherins 4), resulting in a reduction in ER Ca. Meanwhile, PA disrupted the structure and function of mitochondria-associated ER membranes (MAMs) via TGM2 (transglutaminase 2) through the cytosolic Ca-mediated PPP3CB (protein phosphatase 3 catalytic subunit beta)-NFATC2 (nuclear factor of activated T cells cytoplasmic 2) pathway. Further analysis demonstrated that PA induced mitochondrial dysfunction via MAM-mediated mitochondrial Ca insufficiency, thereby restricting mitophagy and attenuating lysosomal acidification. This caused the leakage of mitochondrial reactive oxygen species (mtROS) from depolarized mitochondria into the cytosol via the mitochondrial permeability transition pore, thereby inducing lipid peroxidation, while the addition of ROS scavengers prevented the negative effects of chondrocyte proliferation and hypertrophy and protected chondrocytes from apoptosis in the context of PA. Collectively, PA treatment regulated the proliferation, apoptosis and hypertrophy of antler chondrocytes by disrupting MAM function. - Source: PubMed
Publication date: 2026/09/02
Zhang QiaolingYang ZhanqingYao XueyuanXing YinfeiWang ChenhaoLi BaiyuYue ZhanpengGuo Bin - Transient receptor potential vanilloid channel 3 (TRPV3) is a keratinocyte-expressed ion channel that regulates calcium signaling and thymic stromal lymphopoietin (TSLP) production, contributing to pruritic inflammatory skin diseases. Although avicularin (AVC), a flavonoid from L., and senegenin (SNG), the bioactive aglycone of Willd., possess anti-inflammatory properties, their effects on TRPV3-associated signaling remain unknown. A natural product library was screened for nitric oxide (NO) production in carvacrol-stimulated human keratinocytes. Following primary screening and secondary evaluation of TRPV3 and TSLP expression, AVC and SNG were selected for further study and subsequently evaluated by molecular docking, calcium imaging, quantitative real-time PCR, immunocytochemistry, and pathway inhibition assays. AVC and SNG showed favorable predicted docking poses at both TRPV3 docking sites and significantly attenuated carvacrol-induced calcium-dependent fluorescence responses in TRPV3-expressing cells. Both compounds reduced TRPV3 and TSLP expression at the mRNA and protein levels and attenuated the nuclear translocation of phospho-Nuclear Factor of Activated T Cells 2 (NFATC2) and phospho-p50. Co-treatment with NFAT or Nuclear Factor Kappa B (NF-κB) inhibitors produced no additional suppression, consistent with convergence of AVC/SNG-associated effects with NFAT/NF-κB signaling. Collectively, these findings support further investigation of AVC and SNG as candidate modulators of TRPV3-associated inflammatory signaling in keratinocytes. - Source: PubMed
Publication date: 2026/09/14
Kim Han BiUm Ji YoungSong Da EunChung Bo YoungPark Chun WookKim Hye One - The malignant progression of renal cell carcinoma (RCC) is closely associated with the establishment of an immunosuppressive tumor microenvironment (TME). This study aims to elucidate the oncogenic functions of DNA polymerase ε subunit POLE2 in RCC and its mechanism in modulating the tumor immune microenvironment. We found that POLE2 was significantly upregulated in clear cell RCC (ccRCC) tissues and cell lines. Gain-of-function and loss-of-function experiments demonstrated that POLE2 markedly enhanced tumor cell proliferation, migration, and tumorigenicity both in vitro and in vivo. Mechanistically, POLE2 binds to the PCNA-associated factor PCLAF and stabilizes the PCLAF protein by inhibiting its ubiquitin-proteasome-mediated degradation, thereby leading to increased expression and secretion of SPP1/osteopontin (OPN) in tumor cells. OPN acts as a key cytokine that drives macrophage M2 polarization by activating the CD44/integrin receptors on macrophages and their downstream STAT6 signaling pathway. Moreover, we identified the transcription factor NFATc2 as an upstream regulator of POLE2, which directly binds to the POLE2 promoter and activates its transcription. Our study unveils a comprehensive NFATc2/POLE2/PCLAF signaling axis that promotes ccRCC progression via OPN-mediated M2 macrophage polarization, providing a solid rationale and potential therapeutic targets for developing novel immunocombination therapies. - Source: PubMed
Publication date: 2026/09/22
Li An-RuiXu Jing-WenWu Zhi-HangKang Zhi-JianLuo Run-ShengSu Ya-JuanYuan QiTeng Li-Chen - IL-33 is an alarmine released upon tissue injury. Mast cells (MCs) highly express the IL-33 receptor T1/ST2 (IL-33R) and are thus highly susceptible to released IL-33. Activation of the IL-33R on MCs induces the MyD88-dependent activation of the TAK1-IKK2-p65/RelA signaling pathway, ERK1/2 and p38 which together mediate the production of IL-6, IL-13 and IL-2. Whereas MC-derived IL-6 and IL-13 act as pro-inflammatory cytokines, MC-derived IL-2 acts as an anti-inflammatory cytokine by inducing T cell expansion in vitro and in vivo. The mechanism, which mediate this pleiotropic nature within IL-33-activated MCs is unknown. We hypothesized that precisely balanced signaling pathways define whether MCs act as pro-inflammatory cells by the production of IL-6 and IL-13, or as anti-inflammatory cells by the production of IL-2. Surprisingly, we identified Ca as the determinant factor, which balances the IL-33-induced production of IL-6, IL-13 and of IL-2. Thereby, whereas Ca activates the Calcineurine (CaN)-NFATc2-ERK1/2 signaling pathway, which selectively mediates the production of IL-2, Ca simultaneously limits the activation of p38 and the subsequent production of IL-6 and IL-13 in IL-33-activated MCs. Given that IL-2 producing MCs act as anti-inflammatory cells, our data show that the Ca-CaN-NFATc2-ERK1/2 signaling pathway determines the anti-inflammatory potential of IL-33-activated MCs. - Source: PubMed
Publication date: 2026/09/10
Wagner StellaKüchler ClaudiaHornung KatrinDrube Sebastian - Chronic psychological stress is an environmental factor associated with chronic disease risk and health disparities. Since environmental stressors alter gene expression and physiologic responses through epigenetic mechanisms, perceived discrimination (PD), or the subjective experience of receiving negative treatment related to personal characteristics may influence DNA methylation (DNAm) of CpGs within genes linked to chronic disease. Using the Illumina 850K EPIC chip and psychosocial stress-associated discrimination scales, including the lifetime, racial, and everyday discrimination scales, we identified novel CpGs and differentially methylated positions (DMPs) associated with PD in the context of age, sex, and poverty status among African American and White adults and ones that overlap previous findings of differentially methylated sites (or genes) with discrimination, inflammation, and chronic disease. Ingenuity Pathway Analysis identified several pathways associated with the DNAm patterns and PD with age, sex, and/or poverty status. With age, the white adipose tissue browning pathway was activated among African American participants. This was related to the differential methylation found in the , and genes. Among White participants, the opioid signaling pathway was activated and significantly enriched for the genes , and . Additionally, CpG sites associated with PD among White participants with poverty status revealed that the netrin signaling, opioid signaling, and calcium signaling pathways were activated and significantly enriched for differentially methylated genes, including . The identified novel DNAm genes associated with PD transduce effects through biological pathways related to inflammation and immune response, white adipose tissue browning, and calcium signaling. - Source: PubMed
Publication date: 2026/08/14
Chitrala Kumaraswamy NaiduMoody Danielle L BeattyMode Nicolle AShen BotongHooten Nicole NorenZonderman Alan BEzike NgoziEvans Michele K