NFAT5 Blocking Peptide, Blocking Peptides
- Known as:
- NFAT5 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-9126
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- NFAT5 Blocking Peptide Peptides
Related genes to: NFAT5 Blocking Peptide, Blocking Peptides
- Gene:
- NFAT5 NIH gene
- Name:
- nuclear factor of activated T cells 5
- Previous symbol:
- -
- Synonyms:
- TONEBP, KIAA0827, NFATL1, OREBP, NFATZ, NF-AT5
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-16
- Date modifiied:
- 2019-04-23
Related products to: NFAT5 Blocking Peptide, Blocking Peptides
Related articles to: NFAT5 Blocking Peptide, Blocking Peptides
- Macrophage-driven inflammatory programs and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome plays a critical role for periodontal tissue destruction; however, the transcriptional regulators that mediate these responses remain unclear. This study therefore examined the role of the microRNA-1260b (miR-1260b)-nuclear factor of activated T-cells 5 (NFAT5) axis in inflammatory macrophage responses relevant to periodontal disease. - Source: PubMed
Publication date: 2026/08/04
Hayashi ChikakoFukuda TakaoShida MiyuXiao MengWang ZiyuRyo NaoakiToyoda MasaakiKawakami KentaroShinjo TakanoriAoki TsukasaLi JinfengAhmad MwannnesTaketomi TakaharuUchiumi TakeshiSanui TerukazuNishimura Fusanori - Oral submucous fibrosis (OSF) is a chronic, potentially malignant disorder strongly associated with areca nut chewing. Cuproptosis, a newly identified form of cell death, may play a role in OSF progression, but the mechanisms remain unclear. This study aimed to explore the involvement of cuproptosis in OSF. Here, we observed a significant increase in cuproptosis markers (FDX1 and LIAS) in OSF lesion tissues compared to normal oral mucosa. In vitro, arecoline induced cuproptosis predominantly in epithelial cells, characterized by increased FDX1 and LIAS expression, disrupted lipoylation of DLAT, and elevated intracellular Cu²⁺ accumulation. An epigenetic modification PCR array revealed that arecoline most markedly upregulated PUS1, a pseudouridine (Ψ) modification synthase. Functional knockdown of PUS1 alleviated arecoline-induced cuproptosis, as evidenced by reduced Cu²⁺ levels and restored lipoic acid expression. Dot blot and PA-ψ-seq further demonstrated that arecoline-induced PUS1 upregulation altered the global tRNA pseudouridylation landscape, with enrichment of Ψ peaks in Wnt- and copper transport-related transcripts. PUS1 knockdown markedly attenuated arecoline-induced β-catenin nuclear localization and the upregulation of MYC, FZD6, CTNNB1, NFAT5, SLC25A39, and VDAC2. In conclusion, we reveal a previously unrecognized mechanism whereby arecoline promotes OSF via PUS1-dependent pseudouridylation remodeling and epithelial cuproptosis, offering novel therapeutic targets for OSF intervention. - Source: PubMed
Publication date: 2026/07/27
Lin ShigengDeng WeiWen QitaoXu Xiongjun - Plumage coloration in birds is a complex genetic trait involving both direct pigmentation genes and their modifiers. The Columbian pattern, characterized by black feathers restricted to the neck, wing tips, and tail, remains poorly understood at the genetic level. This study aimed to conduct a genome-wide association study of the Columbian pattern across 29 chicken breeds of diverse origins. Blood samples were collected from breeds with ( = 11) and without ( = 18) the Columbian pattern. Genotyping was performed using the Illumina Chicken 60K SNP chip, and GWAS was conducted using EMMAX with Bonferroni correction. A total of 10 significant and nine suggestive SNPs on chromosomes GGA1, 2, 5, 7, 10, and 11 were identified. Eight significant SNPs mapped to a ~0.7 Mb region on GGA11 containing and multiple functionally diverse genes involved in melanocyte adhesion (), signaling (, ), transcription (, ), protein degradation (, ), and vesicular trafficking (). On GGA2, a significant SNP within a lncRNA gene was located in a QTL for yellow plumage, with positional candidates (, , , , ) suggesting links to pheomelanin deposition. A suggestive locus near on GGA5 was also identified. This study refines the genetic architecture of the Columbian pattern, implicating a core region on GGA11 modulating melanocyte function and a distinct locus on GGA2 involved in pheomelanin synthesis. - Source: PubMed
Publication date: 2026/07/11
Azovtseva Anastasiia IRyabova Anna EShcherbakov Yuri SLarkina Tatiana AVakhrameev Anatoly BDementieva Natalia V - Myasthenia gravis (MG) is an autoimmune disease driven by autoantibodies targeting the neuromuscular junction, leading to muscle weakness. Although emerging evidence implicates circular RNAs (circRNAs) in MG, their specific regulatory mechanisms remain largely unknown. In particular, the role of circNUP214 in MG has not been characterized. CircNUP214 expression in PBMCs and CD4 T cells from MG patients and healthy controls was determined by qRT-PCR. Its circular structure and cytoplasmic localization were verified. Furthermore, the interaction between circNUP214 and miR-31 was confirmed, and the regulatory effect of circNUP214 on CD4 T cell proliferation was evaluated. In 31 pure AChR antibody-positive MG patients, circNUP214 expression was significantly elevated in PBMCs compared with healthy controls (HC). Elevated circNUP214 expression was also observed in CD4 T cells. Functionally, circNUP214 promoted CD4 T cell proliferation, while its knockdown suppressed this process. Mechanistically, circNUP214 directly bound miR-31 and upregulated NFAT5 via sponging miR-31. Rescue experiments in Jurkat cells further validated the circNUP214/miR-31/NFAT5 ceRNA regulatory axis. In conclusion, circNUP214 is highly expressed in PBMCs from 31 pure AChR antibody positive MG patients and is also elevated in CD4 T cells. It upregulates NFAT5 expression by sponging miR-31 to promote proliferation. These findings suggest that the circNUP214/miR-31/NFAT5 axis may contribute to aberrant CD4 T cell proliferation in MG. - Source: PubMed
Publication date: 2026/07/09
Xu FanfanKong XiaotongPeng ShanshanLi LifangTian WenqiCai HanluLi YichenLi YingNiu JingyanZhang NanZhang HuixueWang Lihua - Castration-resistant prostate cancer (CRPC) represents an aggressive stage of prostate cancer that develops following resistance to androgen deprivation therapy. Although androgen receptor (AR) signaling remains a central driver of disease progression, additional adaptive molecular mechanisms contribute to therapeutic resistance. Understanding the transcriptional programs underlying CRPC may facilitate the identification of novel biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/06/25
Naeem Abdulghani AAbdulsamad Saud AHayat AteequllahNaeem AyeshaAlhazmi NadaFallata GhaithBokhari AnasAlharbi Abdulmajeed HAlkinani Kinani AAlshehri Abdullah MAldabbagh Khadijah M