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
- 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 - Ewing sarcoma (ES) and its variants are rare and aggressive malignancies, occurring in paediatric and younger adult populations. Adamantinoma-like ES (ALES) is one of its variants, characterised by fusions, and is exceptionally rare, especially in older adults. There are a few similar cases reported in the literature. We report a rare case of an older adult with a complicated medical history and reported a left neck mass on a follow-up visit; the mass developed over nine months. After evaluation, he was found to have a rare diagnosis of ALES in this age group, specifically with this Ewing Sarcoma RNA binding protein 1 and nuclear factor of activated T cells cytoplasmic 2 () gene fusion. This case highlights the challenges of diagnosing and the multidisciplinary management of rare variants of ES with uncommon gene fusions and raises awareness for the future potential of molecular diagnostics and treatment-specific applications for improved access to care and better outcomes for this population. - Source: PubMed
Publication date: 2026/04/02
Faquih Amber ENoor EemanJawed BilalEwais MennatallahSehbai Aasim - Strategies that specifically target the integrated stress response (ISR) as a therapeutic approach in sepsis remain largely unexplored. This study aimed to identify and validate ISR-related biomarkers in sepsis. - Source: PubMed
Publication date: 2026/03/19
Zhou YouWu YouZhu YuanJiang QinLiu YuZhu LishaZhu RuiCao Haiquan - Intrahepatic cholangiocarcinoma (CCA) is a highly aggressive malignancy arising from the intrahepatic biliary epithelium with insidious onset and dismal clinical outcomes. The lack of reliable early diagnostic markers and effective therapeutic targets underscores the urgent need for novel intervention strategies. Integrated evaluation of public transcriptomic datasets and local validation cohort with survival analysis were performed to assess expression pattern and prognostic significance of cystatin SN (CST1) in CCA. Functional characterization was performed via gain- and loss-of-function experiments in HuCCT1 and RBE cells, complemented by murine orthotopic liver implantation and pulmonary metastasis models. We found that CST1 was significantly upregulated in human CCA tissues. Elevated CST1 expression predicted unfavorable prognosis in CCA patients. Subsequently functional studies revealed that overexpression of CST1 suppressed cellular senescence markers, as evidenced by decreased senescence-associated β-galactosidase activity and downregulated senescence-associated secretory phenotype factors (IL-6, CCL20). Concomitantly, CST1 overexpression enhanced cell proliferation, migration, invasion, and in vivo metastatic capacity. Integrated multi-omics profiling identified CST1-mediated suppression of pyrimidine metabolism through TYMS downregulation. However, exogenous thymidine supplementation failed to rescue proliferation defects upon CST1 knockdown, indicating that CST1-promoted tumor growth is independent of pyrimidine metabolism. Mechanistically, NFATC2 transcriptionally activates CST1, which subsequently abrogates senescence through SOX4 stabilization; ectopic SOX4 expression rescues senescence induced by CST1 depletion. These findings establish CST1 as a promising therapeutic target and provide mechanistic insights for CCA intervention strategies. - Source: PubMed
Publication date: 2026/03/25
Zhao WeiZhao JingLi KunShi JianCong LiyuanYu Guangyi