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
- B cells are key contributors to the pathogenesis of many autoimmune diseases (AID), including multiple sclerosis (MS), and appear to evade the peripheral tolerance checkpoints that normally maintain immune homeostasis. The fate of B cells at these checkpoints is believed to be regulated by intracellular Ca signaling cascades triggered through engagement of B cell receptors (BCR), and by the suppressive effects of regulatory T cells (Tregs). However, most of the current knowledge about Treg-B cell interaction comes from animal studies, while data from human studies, particularly in the context of AID, are sparse. In contrast, impaired Treg-mediated inhibition of conventional T cells (Tcons) has already been described for several AID, including MS. - Source: PubMed
Publication date: 2026/05/02
Greeck Viktoria BWürthwein CorneliaMimura KarinaMattes KatharinaKutza MichaelSchirmer LucasFairless RichardWilliams Sarah KJarius SvenHaas JürgenRuprecht KlemensWildemann Brigitte - - Source: PubMed
Publication date: 2026/04/30
Phuong Tran Thi ThuLong Le HoangUyen Phan Thi TuNhiem Nguyen XuanLee Jeong-HyungDang Nguyen Hai - - Source: PubMed
Publication date: 2026/04/29
Zhang LishanLv YinpingXian GuozheLin Yanliang - Excessive osteoclast activity drives inflammatory bone loss in osteoporosis, rheumatoid arthritis, and periodontitis. Natural compounds represent promising therapeutic candidates with favorable safety profiles; however, few exhibit pathway-biased mechanisms of action. Here, we report that angelic acid (AA), a naturally occurring unsaturated monocarboxylic acid, potently inhibits RANKL-induced osteoclastogenesis. This effect occurs with an IC of 1.9 µM without cytotoxicity. Mechanistically, AA selectively suppressed RANKL-activated phosphorylation of ERK1/2, p38, and JNK (all three MAPK branches), while leaving NF-κB transcriptional activity unaffected. This preferential MAPK suppression disrupted downstream NFATc1 nuclear translocation, thereby preventing NFATc1-driven transcription of osteoclast-specific effector genes including , , and . These findings identify AA as a novel inhibitor of the RANKL-MAPK-NFATc1 axis, providing a mechanistic foundation for its therapeutic development in osteoporosis and other osteolytic diseases. - Source: PubMed
Publication date: 2026/04/17
Zhang LifangTabandeh MojtabaDeepak Vishwa - Interleukin-10 (IL-10) production by B cells plays a critical role in regulating inflammatory responses, yet the mechanisms controlling its expression remain poorly understood. We identified a conserved noncoding sequence (CNS-9) as an essential regulatory element for IL-10 expression in mouse B cells. Comprehensive genomic analyses revealed that CNS-9 functions as an enhancer bound by the transcription factor NFATc1, which facilitates chromatin looping between CNS-9 and the IL-10 promoter to drive transcription. Flow cytometry analyses identified B1a cells as the predominant source of B cell-derived IL-10, with this production critically dependent on NFATc1-mediated CNS-9 regulation. In a mouse model of LPS-induced sepsis, deletion of CNS-9, B cell-specific NFATc1, or both resulted in reduced IL-10 production, exacerbated inflammatory responses, and decreased survival. Furthermore, we demonstrated that the human homolog, CNS-12, functions similarly through NFATc1-dependent mechanisms. These findings establish a conserved regulatory pathway controlling IL-10 expression in B cells with notable implications for inflammatory disease pathogenesis and potential therapeutic interventions. - Source: PubMed
Publication date: 2026/04/24
Kim Seung WonNoh JaegyunPark Hye EunSo Ki HurnHwang WonKim Gi-ChenKim Chan JohngSo Jae-SeonIm Sin-Hyeog