NFAT5 antigen
- Known as:
- NFAT5 antigenic
- Catalog number:
- 'H00010725-Q01-25
- Product Quantity:
- 25
- Category:
- -
- Supplier:
- ACR
- Gene target:
- NFAT5 antigen
Related genes to: NFAT5 antigen
- 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 antigen
'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Anti_Tg)Thyroglobulin Antigen(Des-Asp187)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187)-ME20M_ME20S (185-193) (human, bovine, mouse), (Des-Asp187)-Melanocyte Lineage-Specific Antigen GP100 (185-193) (hu(Des-Asp187,Met186)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187,Met186)-Melanoma-Associated ME20 Antigen (185-193) (human, bovine, mouse), (Des-Asp187,Met186)-95 kDa Melano(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Draxin) C1ORf187, Antigen blocking peptide(Val438)-Tyrosinase (432-444) (human)
(Val438)-LB24-AB (432-444) (human), (Val438)-Monophenol Monooxygenase (432-444) (human), (Val438)-SK29-AB (432-444) (human), (Val438)-Tumor Rejection Antigen AB (0x19 Antigen0x2 Antigen1,25-dihydroxyvitamin D3 Competitive ELISA, Coated with Antigen105 kDa islet cell antigen,BEM-3,Brain-enriched membrane-associated protein tyrosine phosphatase,ICA105,PTP IA-2,PTPLP,Ptprn,Rat,Rattus norvegicus,Receptor-type tyrosine-protein phosphatase-like N,R-P Related articles to: NFAT5 antigen
- 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 - 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
Publication date: 2026/07/21
Chen JiChengFu XinghangGao XiaotanSun YingmingXiao JianChen WenxinWang HebingYang BinglinZhang MaoquanChen YongtianWen YanmeiLuo Huatian - Diabetic foot ulcer (DFU) lacks effective early diagnostic and therapeutic targets. - Source: PubMed
Publication date: 2026/07/21
Liu JinhuaCao LifengWang Xiaxia - Metabolic disorders represent a global health challenge requiring novel therapeutic strategies targeting the gut-liver axis. This study investigates the protective effects and mechanisms of lentinan, a bioactive polysaccharide from , against high-fat diet (HFD)-induced metabolic dysfunction. HFD-fed mice were treated with lentinan. Comprehensive phenotypic assessments, metagenome sequencing, hepatic transcriptomics, and correlation analyses were performed to elucidate mechanisms. Lentinan intervention significantly ameliorated dyslipidemia, hepatic steatosis, systemic inflammation, and intestinal barrier dysfunction in HFD-fed mice. Mechanistically, lentinan induced taxonomically selective gut microbiota remodeling, characterized by substantial enrichment of (positively correlated with hepatic expression) and reduction of (negatively correlated with and ), while paradoxically decreasing despite metabolic improvements. Hepatic transcriptomics revealed significant downregulation of glycerolipid metabolism and oxidative phosphorylation pathways, directly correlating with reduced lipid accumulation and improved serum biochemistry. Unlike conventional prebiotics, lentinan functions as a precision modulator of specific microbial metabolic functions, particularly L-arginine and uridine 5'-monophosphate (UMP) biosynthesis pathways, which interface with host inflammatory and lipid metabolism. These findings establish lentinan as a promising therapeutic candidate for metabolic syndrome management through coordinated gut microbiota-liver axis modulation, providing a conceptual framework for developing precision microbiome-targeted interventions. - Source: PubMed
Publication date: 2026/07/01
Cao DeminHuang LiweiZhang XinyueZhang XinyuZhao ZhiwenLong XidaiZhu XiaoyingLi Yulei - CD8 T cell exhaustion is a conserved differentiation program induced by persistent antigen stimulation and originally characterized in chronic infection. In cancer, this program is actively reinforced and stabilized by the tumor microenvironment. Here, we examine how tumors convert a physiological adaptation to chronic stimulation into a deeply entrenched dysfunctional state. Sustained TCR signaling initiates exhaustion through NFAT- and TOX-dependent transcriptional remodeling, but tumor-specific extrinsic pressures, including hypoxia, metabolic competition, ionic imbalance, mechanical stress, and heterogeneous antigen exposure, amplify and stabilize this program. These environmental cues converge on transcription factor networks such as IRF, BATF, NR4A, and NFAT5, which integrate chronic signaling with stress-adaptive responses and progressively restrict effector potential. Exhaustion in tumors becomes epigenetically imprinted. Exhaustion-specific enhancer landscapes persist despite PD-1 blockade, reflecting a lineage-like state enforced by chromatin remodeling factors such as TOX. Thus, checkpoint inhibition transiently restores function without fully reprogramming cellular identity. We propose that tumor-induced exhaustion arises from the layered convergence of chronic antigen signaling and microenvironmental reinforcement, culminating in chromatin fixation. Understanding this stabilization process reframes therapeutic strategies: effective cancer immunotherapy will likely require combinatorial approaches that target not only inhibitory receptors but also metabolic resilience, stress-sensing pathways, and epigenetic architecture. By dissecting how tumors convert adaptive restraint into durable dysfunction, new avenues may emerge to destabilize exhaustion and restore durable antitumor immunity. - Source: PubMed
Publication date: 2026/06/26
Thouenon RomaneOngaro MarcoVerdeil Grégory