Ask about this productRelated genes to: NFATc2 antibody
- 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 antibody
Related articles to: NFATc2 antibody
- Malignant melanoma remains a formidable clinical challenge due to its propensity for metastasis and therapeutic resistance. Identifying molecular targets that regulate malignant melanoma progression is critical for developing effective therapies. In this study, we investigated the role of cysteine-rich intestinal protein 1 (CRIP1), a novel oncogene, in melanoma progression. CRIP1 expression was analyzed using public datasets, and functional roles of CRIP1 in proliferation, colony formation, migration, and invasion were assessed via overexpression cell models. Mechanistic insights were gained through RNA sequencing, bioinformatics, 4-phenylbutyric acid (4-PBA) or N-acetylcysteine (NAC) treatment, Western blot, dual-luciferase reporter, and chromatin immunoprecipitation (ChIP). Xenograft models were used to confirm in vivo effects. CRIP1 was significantly upregulated in melanoma tissues, particularly in metastases, and correlated with an endoplasmic reticulum (ER) stress gene signature. CRIP1 overexpression promoted malignant phenotypes in vitro and tumor growth in vivo, which was dependent on the activation of ER stress. Integrative analysis identified SREBF1 (Sterol Regulatory Element Binding Transcription Factor 1) as a downstream target. CRIP1 increased intracellular ROS levels by promoting SREBF1 expression, thereby activating ER stress and promoting malignant phenotypes in melanoma cells. Mechanistically, CRIP1 promoted NFATC2 (nuclear factor of activated T cells 2) binding to the SREBF1 promoter to drive transcription of SREBF1. These findings indicate that CRIP1 serves as a critical driver of melanoma progression through ER stress activation and identify a novel CRIP1/NFATC2/SREBF1 axis, providing insights into the role of CRIP1 in melanoma biology and presenting new potential therapeutic targets for this aggressive malignancy. - Source: PubMed
Publication date: 2026/05/13
Yu TingSu YongfengZou Ping'anJian YanWang Yaqi - Renal tubulocystic oncocytoma (RTO) is an exceptionally rare variant of renal oncocytoma (RO) with poorly understood genetic underpinnings. This study aimed to characterize the clinicopathological features and genomic landscape of RTO to enhance diagnostic precision and elucidate its molecular profile. - Source: PubMed
Publication date: 2026/04/14
Wang WenchiZhu HengxingChen ChunyuSun ManWang HonglongTai YuChen SishanLiu ZhuoFan BoLi Yinghua - Transcription factor nuclear factor of activated T cells (NFAT) plays a central role in immune gene regulation through cooperative interactions with diverse transcriptional partners. While FOXP family members have been identified as co-regulators of NFAT1, the involvement of other FOX family proteins has remained mechanistically obscure. Here, we solved three crystal structures of NFAT1-RHR/FOXC2-DBD/ARRE DNA ternary complexes and uncovered an unexpected mode of transcriptional repression mediated by FOXC2 through direct, DNA-facilitated binding to the V-shaped groove of NFAT1's Rel-homology region (RHR). Biochemical assays revealed that DNA enhanced FOXC2-NFAT1 interaction by more than five-fold, supporting a model in which DNA acts as a structural co-factor that promotes complex formation. Mutational disruption of the FOXC2-NFAT1 interface impaired complex assembly and abrogated transcriptional repression. Functional assays further confirmed that FOXC2 suppressed NFAT1-driven transcription of multiple cytokines and chemokines, including IL2, TNF, CXCL5, and CCL2. Notably, this repressive mechanism was found to extend to other FOX proteins (FOXI1, FOXO1, and FOXK1), suggesting a broader paradigm of FOX-NFAT1 interaction. Our study defined a previously unrecognized FOX-mediated transcriptional repression mechanism and provides a structural framework for NFAT inhibition by FOX proteins, offering novel insights into the transcriptional regulation of immune-related genes. - Source: PubMed
Chen XiaojuanWu SipengYue SitongZhang LinLiu XueruDai ShuyanLi JunZhang HuajunWei HudieGuo MingQu LingzhiChen LinDeng YalanChen Yongheng - When migratory cells move between stiffness niches in vivo, they encounter confined spaces imposed by extracellular matrix (ECM) networks. Cells from one niche possess mechanosensitive adaptations that influence their response to new environments, a concept known as mechanical memory. How this memory is acquired and how it influences migratory potential in confinement remain poorly understood. Here, we combine stiffness priming using polyacrylamide hydrogels with a confinement platform to screen memory across healthy and transformed cells. Using a dose-and-passage approach, we find that cells primed on soft substrates navigate confinement more efficiently. Bulk RNA sequencing identifies NFATC2 as a transcription factor mediating mechanical memory through genetic reprogramming. Inhibition of NFATC2 confirms that it is required for memory acquisition and enhanced confined migration. Highly invasive cancer cells fail to retain mechanically induced phenotypes following cue removal, suggesting differential adaptation strategies. These findings establish mechanical memory as a cell-intrinsic regulator of confined migration. - Source: PubMed
Publication date: 2026/04/16
Lee Jia Wen NicoleChang YejiChitnis Malhar SLi YixuanGao XuSun Avery RuiZhu JinYoung Jennifer LHolle Andrew W - Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes synovial inflammation and joint injury. Currently, safe multitargeted therapies for RA are lacking. Fangfeng Decoction (FFD), a 1,800-year-old traditional Chinese medicine, has been shown to relieve the symptoms of RA in clinical practice; however, its experimentally verified modern pharmacological mechanisms of action remain unclear. - Source: PubMed
Publication date: 2026/04/10
Shi LiliShen ZhongfeiShen BinXu YuanyuanShao LiangWu MinJiang XiaohongDong Jingjian