TXNIP_RAT Txnip ELISA tesk kit
- Known as:
- TXNIP_RAT Txnip Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15152
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- TXNIP_RAT Txnip ELISA tesk kit
Related genes to: TXNIP_RAT 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
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- Mucosal inflammation is the defining feature of ulcerative colitis (UC), which is a chronic inflammatory bowel disease. The goal of this study was to determine the involvement of the TXNIP/NLRP3 inflammatory pathway in UC development and to assess the therapeutic potential of engeletin and rosuvastatin. Acetic acid (AA) was used to initiate UC. The animals were divided into seven groups: normal control, UC control, UC treated with mesalazine (100 mg/kg/day), UC treated with rosuvastatin (20 mg/kg/day), UC treated with engeletin (25 mg/kg/day), UC treated with engeletin (50 mg/kg/day), and UC treated with a combination of rosuvastatin and engeletin (20 mg and 25 mg/kg/day). All treatments lasted 21 days. Body weight, colon weight, colon length, and weight-to-length ratio were all assessed. ELISA was used to detect IL-1β, MPO, gasdermin-D, NF-κB p65, and TXNIP contents. TXNIP expression was quantified by quantitative real-time PCR, and colon samples were examined histopathologically and immunohistochemically. UC caused significant weight loss, increased colon weight, and a shift in the colon weight-to-length ratio. These changes were associated with elevated inflammatory markers and upregulation of the TXNIP/NLRP3 pathway markers. All measured parameters were significantly improved after treatment with engeletin, rosuvastatin, and their combination, with the combination having the most pronounced therapeutic benefits. In conclusion, this study demonstrated that AA-induced UC was associated with increased expression of TXNIP/NLRP3-related inflammatory markers, which may contribute to the disease pathophysiology. The combination of engeletin and rosuvastatin was associated with downregulation of TXNIP/NLRP3-related inflammatory signaling and amelioration of biochemical and histopathological changes associated with UC. - Source: PubMed
Publication date: 2026/08/24
El-Masry Thanaa AAbu-Risha Sally ENegm Walaa AA Kamal Eman - TXNIP and DYRK1A are two novel drug targets for the treatment of type 2 diabetes (T2DM), and their respective inhibitors have been shown to suppress islet β-cell apoptosis and promote islet β-cell proliferation. The quinazoline scaffold constitutes the core pharmacophore of TXNIP inhibitors. Harmine, a prototypical DYRK1A inhibitor bearing a β-carboline scaffold, has demonstrated robust β-cell proliferative activity. Carbazole serves as a structurally simplified bioisostere of β-carboline. Guided by the principles of multi-target drug design and combinatorial chemistry, we designed and synthesized a series of quinazoline-carbazole hybrids as dual TXNIP/DYRK1A inhibitors. Compounds PF-5 and PF-6 markedly attenuated palmitic acid (PA)-induced β‑cell injury by suppressing the TXNIP-NLRP3-IL-1β signaling axis. Meanwhile, compounds PF-6 and PF-8 enhanced β-cell proliferation via DYRK1A inhibition. Molecular docking confirmed PF-6 bound with high affinity to both targets, and ADMET predictions supported its drug-like properties. Thus, PF-6 emerges as a potential dual-target therapeutics for T2DM. In conclusion, PF-6 can be used as a potential new chemical entity against T2DM. - Source: PubMed
Publication date: 2026/08/22
Guan LiSu WanzhenMi ZhuWang JingLi YananSong PengfeiHan WenxiaBai TongxuanFei WenlingLao KejingLi XiaochengLi AiyunLi Weize - Post-transcriptional gene regulation is central to maintaining cellular homeostasis. Among its mechanisms, alternative splicing (AS) fine-tunes cellular adaptation to stress. This study employed an approach combining RNA splicing analysis with RNA-binding protein (RBP) motif enrichment in primary osteocytes cultured in high-glucose conditions. Our analysis identified the RBP human antigen R (HuR) as a top candidate associated with AS regulation. Loss of HuR reshaped the transcriptome through gene expression and splicing changes, converging on two major pathways: stress response and translational control. Functional validation revealed that HuR depletion heightened oxidative stress, impaired mitochondrial function, and rewired key translational signals, while preserving global protein output. Mechanistically, we identified TXNIP mRNA-protein uncoupling following HuR knockdown (KD), characterized by elevated mRNA but reduced protein expression. Collectively, these findings support HuR's role as a key post-transcriptional regulator of osteocyte metabolic adaptation under high-glucose stress, with potential implications for hyperglycemic bone fragility. - Source: PubMed
Publication date: 2026/08/10
Fan ZiqiuMarahleh AseelKitaura HidekiRen JiayiMousa AbdulrahmanOhori FumitoshiNiizuma KuniyasuRashad SherifKanetaka Hiroyasu - Age-related osteoporosis is shaped by disrupted bone remodeling, metabolic stress, and inflammation. We combined an exploratory clinical comparison in adults aged 65 years and older with a D-galactose aging rat model and osteoblast-like cell experiments to examine exercise-associated changes in trimethylamine N-oxide (TMAO) and inflammasome signaling. Higher habitual activity in older adults was associated with higher hip T scores, lower serum and fecal TMAO, reduced IL-18 and IL-1β, and a turnover profile favoring bone formation. In aged rats, exercise lowered circulating and femoral marrow TMAO, preserved trabecular architecture, improved maximal load, and restrained TXNIP NOD-like receptor family pyrin domain-containing 3 (NLRP3) signaling while maintaining alpha Klotho. In osteoblast-like cells, TMAO promoted senescence and inflammasome assembly, whereas pathway modulation reduced these effects. These data support a gut bone inflammatory framework for exercise-associated skeletal protection in aging. - Source: PubMed
Publication date: 2026/08/11
Zhang LihuaHuang XiaoyuZhang JiaweiSi XiangyueZuo HongchunWang QunGong Weijun - Diabetic kidney disease (DKD) is a major cause of renal failure and end-stage renal disease. Pyroptosis, a Gasdermin-dependent inflammatory form of programmed cell death, has been implicated in DKD progression. Metformin has shown renoprotective effects in DKD; however, the underlying mechanisms remain unclear. - Source: PubMed
Publication date: 2026/08/19
Shi ShuyuWang BingZhou YangLi QiHou YushengZhang XinyiWang Qiuyue