Mouse polyclonal to NFAT5, Host Mouse
- Known as:
- Mouse pab NFAT5, Host Mouse
- Catalog number:
- YF-PA17176
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal NFAT5 Host
Related genes to: Mouse polyclonal to NFAT5, Host Mouse
- 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: Mouse polyclonal to NFAT5, Host Mouse
Related articles to: Mouse polyclonal to NFAT5, Host Mouse
- 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
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Naeem Abdulghani AAbdulsamad Saud AHayat AteequllahNaeem AyeshaAlhazmi NadaFallata GhaithBokhari AnasAlharbi Abdulmajeed HAlkinani Kinani AAlshehri Abdullah MAldabbagh Khadijah M - Breast cancer remains a leading cause of cancer-related mortality worldwide, with triple-negative breast cancer (TNBC) representing a particularly aggressive subtype lacking targeted therapies. Inducing copper-mediated cell death stands as a significant therapeutic approach for tumors; however, research into non-coding RNA regulation of copper-mediated cell death in TNBC remains relatively scarce. This study analyses transcriptomic data from TNBC patients to identify long non-coding RNAs (lncRNAs) associated with copper-mediated cell death, aiming to uncover potential therapeutic targets. - Source: PubMed
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