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
- The mechanisms that predispose dopaminergic neurons (DAN) to degeneration in Parkinson's disease (PD) are incompletely understood. - Source: PubMed
Publication date: 2026/08/18
Macchi MircoGinolhac AurélienHeurtaux TonyGomez-Ramos BorjaSinkkonen LasseGlaab Enrico - Acute lung injury arising from acute pancreatitis or sepsis remains a major clinical challenge and lacks specific therapeutic strategies. Neutrophil activation and infiltration, tightly governed by intracellular Ca signaling via ORAI1-based Ca release-activated Ca (CRAC) channels, play central roles in the pathogenesis of acute lung injury. Here, we engineered a neutrophil-targeted lipid nanoparticle (neutLNP) encapsulating the selective CRAC channel inhibitor CM4620 (Anti-Ly6G@CM4620-LNP) for intranasal delivery. The neutLNP efficiently suppressed neutrophil chemotaxis and reactive oxygen species production, and significantly attenuated lung injury in both pancreatitis- and sepsis-associated lung injury models. Compared with intranasally administered free CM4620, neutLNP produced greater reductions in selected histological and inflammatory endpoints. Pulmonary imaging and flow cytometry demonstrated distribution within the inflamed lung parenchyma and preferential association with pulmonary neutrophils, whereas pharmacokinetic analysis showed markedly lower plasma CM4620 exposure after intranasal than after intraperitoneal administration. Mechanistically, integrated transcriptomic and single-cell proteomic profiling of pulmonary neutrophils from neutrophil-specific Orai1-deficient mice identified CD166 as a downstream mediator of ORAI1 signaling. Further analyses showed that ORAI1 signaling transcriptionally promotes CD166 expression, at least in part through NFATc2. Together, these findings support intranasal neutLNP delivery as a locally directed strategy that enhances lung protection relative to intranasal free CM4620 while limiting systemic exposure compared with intraperitoneal delivery, and establish CD166 as a functionally important downstream mediator of ORAI1-dependent neutrophil adhesion in acute inflammatory lung injury. - Source: PubMed
Publication date: 2026/08/12
Yang ZihanMeng QingyeZhu LiuQiu BintaoChen YonghaoLu WanyiZhang XiuliPeng KaixinWong Catherine C LWu DongWen Li - Persistent antigenic stimulation leads to the dysfunction of CD8 cytotoxic T cells. These "exhausted" T cells exhibit reduced proliferative capacity, impaired effector function, and increased expression of co-inhibitory receptors. Chronic antigen receptor stimulation induces the expression of NFATc1/αA, a short isoform of NFATc1 that promotes T cell survival. The induction of NFATc1/αA is accompanied by a significant decrease in NFATc2 expression. NFATc2 limits the expression of stemness-associated genes, such as , , and It also supports the expression of , , and the T marker gene . Therefore, ablation of NFATc2 mitigates functional exhaustion of CD8 T cells during chronic viral infection and antitumor immunity. Our findings illustrate that NFATc1 promotes the survival of T cells, while NFATc2 promotes the terminal differentiation and dysfunction of exhausted CD8 T cells. The data suggest a non-redundant interplay between NFATc1 and NFATc2, each playing a distinct role in controlling CD8 T-cell exhaustion. These findings open novel avenues to enhance the efficacy of immune checkpoint and CAR T-cell therapies. - Source: PubMed
Publication date: 2026/07/24
Sampere-Birlanga SalvadorKlein-Hessling StefanCampillo Prados MiriamHuang AnfeiWu HaoRosenwald AndreasKastenmüller WolfgangSerfling EdgarVaeth MartinBerberich-Siebelt Friederike - Melanoma plasticity drives immune evasion and therapy resistance through dynamic cell-state transitions beyond genetic alterations. Although epigenetic remodeling is central to this process, its impact under therapeutic pressure remains unclear. We profiled longitudinal biopsies from patients with melanoma treated in the phase 1b NIBIT-M4 epi-immunotherapy trial [NCT02608437, DNA (cytosine-5)-methyltransferase 1 inhibitor plus anti-CTLA-4] using single-cell multiome and spatial transcriptomics. Seven malignant meta-programs were identified, including a rare Wnt/β-Catenin melanocytic state and a dedifferentiated neural crest-like state enriched in nonresponders. Spatial analyses showed that homotypic clustering stabilizes resistant programs, with neural crest-like cells forming compact niches. Responders displayed enrichment of antigen presentation/interferon program and coordinated T and B cell expansion, whereas nonresponders retained stable neural crest-like clusters. Epigenetic therapy reactivated transposable elements, priming innate immunity and enhancing immunogenicity. Nuclear factor of activated T cells, cytoplasmic 2 (NFATC2) emerged as a master regulator of neural crest-like states and resistance; its perturbation promoted differentiation and immunogenicity. These findings define mechanisms of resistance and nominate β-Catenin and NFATC2 as therapeutic vulnerabilities. - Source: PubMed
Publication date: 2026/08/07
Ciervo ErikaCeccarelli FrancescoDi Giacomo Anna MariaGrisolia PieraCovre AlessiaBesharat Zein MersiniDe Falco AntonioCaruso Francesca PiaLaezza LuigiFerraro LuigiMartin Gloria MasBilbao DanielWilliams SionCurrall BenjaminLofiego Maria FortunataSani TommasoFerretti ElisabettaGuo YanHolden Sean BSimeone InesMortarini RobertaAnichini AndreaMaio MicheleNoviello Teresa Maria RosariaCeccarelli Michele - Bone and soft tissue sarcomas harboring EWSR1::NFATC2 and FUS::NFATC2 fusions (NFATC2-rearranged sarcomas) is a recently defined entity with a morphologic spectrum and clinical behavior that are not fully elucidated. We studied 32 such sarcomas that occurred in 21 male and 11 female patients. The EWSR1::NFATC2 fusion was found in tumors of 25 patients (17 M, 8 F; median age: 40, range: 14-78), 16 of which arose in soft tissue, while 8 originated in bone. Morphologically, they showed relatively consistent morphologic features yet variable degrees of cytologic atypia, mitotic rates and necrosis. Follow-up (19 patients; median: 22 months, range: 1-70) demonstrated local recurrence in 3 patients, while distant metastases occurred in 6 patients. Two patients died of disease (DOD), 4 were alive with disease (AWD) and 13 were without evidence of disease (AWOD). In contrast, the FUS::NFATC2 fusion was exclusively seen in osseous tumors, which occurred in 7 patients (4 M, 3 F; median age: 32, range: 4-62). Further, FUS::NFATC2 tumors showed significant morphologic heterogeneity. Follow-up (6 patients; median: 18 months, range: 13-60) demonstrated local recurrence in 2 patients, and lung metastases in 2 patients. At last follow-up, 3 patients were AWD, while 3 patients were AWOD. Using a two-tiered grading scheme based on cytologic atypia, mitotic rate, and necrosis, patients with low-grade tumors experienced significantly fewer adverse events than those classified as high-grade (p=0.026); however, estimated metastasis-free survival was not statistically significant due to our limited sample size. Overall, our study expands on the morphologic spectrum of NFATC2-rearranged sarcomas and highlights the clinicopathologic, molecular, and genetic differences between the EWSR1- and FUS-rearranged tumors. Although additional long-term follow-up data is required, our study further suggests that a subset of these sarcomas have a protracted clinical course while high-grade morphologic features such as atypia, mitotic activity and necrosis may correlate with worse behavior. - Source: PubMed
Publication date: 2026/08/03
Torres-Mora JorgeDehner Carina AWarmke Laura MFolpe Andrew LChrisinger John S ADemicco Elizabeth GDickson Brendan CGross John MBishop Justin AGupta SounakBuehler DaryaKipp BenjaminMichal MichaelIding Jeffrey StephenHalling Kevin CWenger Doris EPujari Ganesh PAlvand SabaFritchie Karen J