TXNIP_HUMAN TXNIP ELISA tesk kit
- Known as:
- TXNIP_HUMAN TXNIP Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15142
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- TXNIP_HUMAN TXNIP ELISA tesk kit
Related genes to: TXNIP_HUMAN TXNIP ELISA tesk kit
- Gene:
- TXNIP NIH gene
- Name:
- thioredoxin interacting protein
- Previous symbol:
- -
- Synonyms:
- VDUP1, EST01027, HHCPA78, THIF, ARRDC6
- Chromosome:
- 1q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-12
- Date modifiied:
- 2016-10-05
Related products to: TXNIP_HUMAN TXNIP ELISA tesk kit
Related articles to: TXNIP_HUMAN TXNIP ELISA tesk kit
- Osteoarthritis (OA) primarly involves the degradation of joint cartilage and requires new treatments. REJENERA, a newly developed nutraceutical formula against OA, contains primarily olive leaf bioflavonoids ( ZeyEX, quercetin and luteolin), S-allylcysteine, palmitoylethanolamide, L-proline, hyaluronic acid and boron. This study focuses on the efficacy of REJENERA in treating knee OA and aims to compare it with ZeyEX, NPROC (a product obtained by combining collagen-rich eggshell membrane with olive leaf extract), and IBUPROFEN in a rat OA model. OA was established by intra-articular injection of monosodium iodoacetate (MIA; 3 mg) into the right knee joints. Rats were either left untreated or treated orally for 12 weeks with REJENERA, ZeyEX, NPROC (300 mg/kg/day) or IBUPROFEN (3 mg/kg/day). MIA injection produced joint degeneration including increased fissure-index, osteophyte-score, and OARSI-score, joint swelling, synovial inflammation, proteoglycan loss, and decreased cartilage thickness. These histopathological abnormalities were partially but significantly alleviated by REJENERA and other treatments. Only ZeyEX significantly inhibited the OA-induced increase in IL-1β, IL-6, IL-10 and LPO in serum, and IL-6, TNF-α, and IFN-γ in synovial fluid. While increases in MMP-3 and MMP-9 were reduced with all treatments, MMP-13 was inhibited only by REJENERA. ZeyEX increased IL-2, NPROC increased IL-6, and IBUPROFEN inhibited IL-10. All treatments improved TIMP-1 levels; however, TXNIP was more significantly inhibited by ZeyEX, and NLRP3 by REJENERA. REJENERA's anti-OA effects are accompanied by an increase in cartilage anabolic factors (Ki-67, type-II collagen, BMP-7) and inhibition of apoptosis. REJENERA offers a promising multi-targeted therapeutic approach to treating OA by blocking the iNOS-TXNIP-NLRP3 signaling axis, and reducing oxidative stress. - Source: PubMed
Publication date: 2026/07/06
Tepedelenlioglu Huseyin EmreElmazoglu ZubeyirSaribas Sanem GulistanTutuncu YildizCeylan Asli FKarasu Çimen - Asthma is a chronic inflammatory airway disease. Thioredoxin-interacting protein (TXNIP), a thioredoxin (TRX)-binding protein, is involved in the regulation of inflammatory responses and apoptosis. The NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome is a key mediator of inflammatory responses. MicroRNAs (miRNAs) are small non-coding RNAs. Previous studies have demonstrated that expression is significantly downregulated in bronchial epithelial cells of asthmatic rats. However, whether regulates the NLRP3 signaling pathway by targeting TXNIP and thereby influences airway inflammation in asthma remains unclear. This study aims to investigate the mechanism by which alleviates ovalbumin (OVA)-induced airway inflammation in asthmatic rats through regulation of TXNIP and suppression of the NLRP3 signaling axis. - Source: PubMed
She WeiweiShe MingdeSun TianshouChen XuWang MingdongZhang RaoyiFang HuanhuanLi YanmeiChen Meiyu - Intervertebral disc degeneration (IVDD) is a major cause of low back pain, characterized by extracellular matrix breakdown, loss of hydration, and disc height. Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, is implicated in IVDD pathogenesis, but the upstream signals in disc cells remain unclear. Advanced oxidation protein products (AOPPs), oxidative stress-derived protein modifications, accumulate in degenerating discs and activate NADPH oxidase 4 (NOX4), a critical regulator of reactive oxygen species (ROS) and ferroptosis. We hypothesize that AOPPs induce ferroptosis in disc cells via NOX4 activation. In our study, using a rat puncture-induced IVDD model, intradiscal administration of AOPPs exacerbated IVDD, as shown by decreased disc height, higher Pfirrmann grade, matrix degradation, and upregulation of NOX4, TXNIP, and FTH, alongside downregulation of GPX4. In vitro, AOPPs and the ferroptosis inducer Erastin induced ferroptotic changes in nucleus pulposus and annulus fibrosus cells, including elevated MDA, iron overload, GSH depletion, mitochondrial shrinkage, and altered ferroptosis-related proteins, which were reversed by Ferrostatin-1. Pharmacological inhibition or genetic knockdown of NOX4 attenuated AOPPs-induced ferroptosis in vitro and protected against IVDD in vivo. Our results highlight NOX4 as a central regulator in AOPPs-induced ferroptosis, promoting IVDD, and suggest that targeting NOX4 to inhibit ferroptosis may offer a novel therapeutic strategy against IVDD. - Source: PubMed
Publication date: 2026/07/02
Tu KewuZhao KunLiao DongtengChen ZhaomouXu FuzhouLu WeiqiChen YuLiu ZhongyuanLiao CongruiYu ZihanZhou BeidiDai Xiangheng - Hypertension is linked to a shortened erythrocyte lifespan, with endothelial cells acting as non-professional phagocytes to clear senescent erythrocytes. However, whether increased erythrophagocytosis contributes to endothelial inflammation remains unclear. Frataxin (FXN) plays a crucial role in controlling iron balance and metabolism. This study investigated the role of FXN-mediated iron engulfment in regulating endothelial pro-inflammatory phenotype. - Source: PubMed
Publication date: 2026/07/02
Cheng XingyiCheng YiHuang ChenglinWei TongGuo YuetongGao JingShen Weili - Hypoxia disrupts corneal physiological function by impairing energy metabolism. We identify AMP-activated protein kinase (AMPK) as a central regulator of coordinated metabolic adaptation in the hypoxic cornea. Using human corneal epithelial cells and an alkali burn-induced mouse model of corneal hypoxia, we combined metabolic flux analysis, mitochondrial morphology assessment and pathway-specific pharmacological and molecular approaches to characterize AMPK-dependent metabolic regulation. We demonstrate that hypoxia-induced AMPK activation is not merely a stress response but an essential driver of metabolic adaptation. Importantly, we found that AMPK coordinates bidirectional metabolic reprogramming. It enhances glycolytic flux through the AMPK/TXNIP/GLUT1 axis and improves mitochondrial oxidative capacity by regulating mitochondrial biogenesis via PGC1α, mitochondrial dynamics via MFF/DRP1 and MTFR1L/OPA1, and mitophagy via ULK1. This coordinated regulation of fuel supply and energy production suggests an integrative role of AMPK in the corneal epithelium. Pharmacological activation of AMPK with AICAR recapitulated this coordinated response, restored energy homeostasis, and mitigated hypoxic damage. Our findings indicate AMPK as a important regulator of glycolysis and mitochondrial function in the hypoxic cornea, highlighting a metabolic network with therapeutic potential. By demonstrating that AICAR rescues corneal energy failure through this dual mechanism, our findings support a potential metabolic restoration strategy that extends beyond single-pathway targeting and may provide a new approach for treating corneal diseases associated with metabolic dysregulation. - Source: PubMed
Publication date: 2026/07/02
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