ENPL_BOVIN HSP90B1 ELISA tesk kit
- Known as:
- ENPL_BOVIN HSP90B1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen12049
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- ENPL_BOVIN HSP90B1 ELISA tesk kit
Related genes to: ENPL_BOVIN HSP90B1 ELISA tesk kit
- Gene:
- HSP90B1 NIH gene
- Name:
- heat shock protein 90 beta family member 1
- Previous symbol:
- TRA1
- Synonyms:
- GP96, GRP94
- Chromosome:
- 12q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-03
- Date modifiied:
- 2016-10-11
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- Fluorosis can induce cognitive dysfunction. The cognitive impairment caused by fluorosis is closely related to endoplasmic reticulum stress (ERS) and abnormal lysosomal acidification. However, the specific molecular mechanism is not known, and effective intervention strategies are lacking. Diterpene ginkgolides meglumine injection (DGMI) is used clinically as a neuroprotective agent, but whether it can inhibit ERS, regulate lysosomal acidification, and ameliorate fluorosis-induced cognitive dysfunction merits investigation. - Source: PubMed
Chen RuiXie PengFan XinruiZhou ZihangMu ChunyanJi Qiuhong - Exposure to hydrochloric acid (HCl) can provoke severe chronic pulmonary injury. Children are particularly vulnerable due to their smaller airways, higher respiratory rate, and stronger inflammatory response; yet no countermeasures exist for HCl-induced chronic lung injury in the pediatric population. We have previously demonstrated the involvement of HSP90 during HCl-induced lung injury in pre-pubertal (p24) mice, who develop stronger persistent inflammation with higher NLRP3 inflammasome activation, but less pulmonary fibrosis compared to adults. Here, we tested the hypothesis that post-treatment with the second-generation HSP90 inhibitor AT13387 (Onalespib), administered subcutaneously beginning 24 h after HCl instillation, would prevent HCl-induced chronic lung injury and pulmonary fibrosis in young (p24) C57BL/6J mice. Pre-pubertal (p24) C57BL/6J mice received a single intratracheal instillation of 0.1 N HCl and were treated with AT13387 (10 mg/kg, s.c., 3×/week for 30 days) beginning 24 h post-exposure. Bronchoalveolar lavage fluid (BALF) analysis, lung function measurements, histological assessment (Ashcroft fibrosis score), and Western blot analysis of key signaling mediators were performed. Additionally, publicly available single-nucleus RNA sequencing (snRNA-Seq) data from a cohort of 13 infants with bronchopulmonary dysplasia (BPD) and 11 age-matched controls were analyzed to evaluate HSP90 isoform expression in human pediatric lung disease. AT13387 significantly reduced BALF white blood cell concentration without affecting total BALF protein levels. Importantly, AT13387 did not impair normal weight gain or development over the 30-day observation period. AT13387 abrogated HCl-induced expression of TGF-β1, phosphorylation of HSP90, ERK1/2, SMAD2, IκBα, and upregulation of the inflammasome NLRP3. Additionally, AT13387 prevented changes in lung function dynamics and reduced the Ashcroft fibrosis score. Analysis of the human snRNA-Seq BPD dataset revealed a widespread pan-overexpression of all three HSP90 isoforms, i.e., HSP90AA1, HSP90AB1, and HSP90B1. These findings suggest that the HSP90 inhibitor AT13387 exhibits strong antidotal properties against HCl-induced chronic lung injury and pulmonary fibrosis in a pre-clinical pediatric model and identify HSP90 as a conserved therapeutic target in pediatric chronic lung disease. - Source: PubMed
Publication date: 2026/09/11
Solopov Pavel ADimitropoulou ChristianaCatravas John DColunga Biancatelli Ruben M L - This study investigated the ability of quercetin (QU) alone or with sildenafil (Sild) or pentoxifylline (PTX) to modulate carbon tetrachloride (CCl)-induced renal fibrosis in Wistar albino rats. Renal fibrosis was induced by intraperitoneal injection of CCl (1.5 ml/kg, three times weekly for 10 weeks). Rats received oral doses of QU (50 mg/kg once daily), PTX (50 mg/kg once daily), and Sild (10 mg/kg twice daily) separately or in combination from week 7 to week 10. CCl induced severe renal injury as indicated by urinary electrolytes disturbance, renal function impairment, increased oxidative stress, inflammation, up-regulation of endoplasmic reticulum (ER) stress markers (CHOP, GRP75), and apoptosis (Bax), as well as down-regulation of defense proteins (Bcl2, Nrf2, HO-1). QU, Sild, and PTX, alone or in combination, improved renal function and alleviated histological changes. The combination of QU with Sild or PTX resulted in greater renoprotection by regulating several key pathways, including reductions in ER stress, enhanced antioxidative defenses, and regulation of apoptosis. In conclusion, a combination of QU with Sild or PTX ameliorates renal fibrosis by inhibiting ER stress-induced cellular apoptosis through modulation of the GRP75/CHOP/Bax/Bcl2 and oxidative stress pathways. - Source: PubMed
Publication date: 2026/09/24
Nasr GehadAli Doaa Mohamed ElrobyFawzy Michael AAli Fares E MFathy Moustafa - Cancer-associated fibroblasts (CAFs) shape bladder cancer progression, but functionally relevant CAF-associated drivers remain insufficiently characterized. This study aimed to identify CAF-enriched genes with translational relevance and to determine whether GLG1 mediates tumor-stromal crosstalk in bladder cancer. Single-cell RNA sequencing from bladder cancer tissues was integrated with Mendelian randomization, Bayesian colocalization, correlation analyses, immunostaining of clinical specimens, CAF-conditioned medium assays, GLG1 knockdown/overexpression, TGF-β1/Smad2/3 assessment, and xenograft modeling. Single-cell profiling of nine bladder cancer samples retained 60,561 cells and identified fibroblast-enriched transcriptional programs. Among 960 fibroblast-enriched genes, Mendelian randomization identified 22 genes whose genetically predicted expression was associated with bladder cancer risk, and colocalization prioritized GLG1, HES4, and HSP90B1. GLG1 was selected for validation because it showed fibroblast-enriched expression, genetic support for bladder cancer association, and shared cis-eQTL/GWAS signals. GLG1 expression was higher in tumor tissues than in adjacent normal tissues, consistent with a stromal localization pattern, and GLG1 positivity was associated with tumor invasiveness. Tumor-derived TGF-β1/Smad2/3 signaling contributed to GLG1 upregulation in fibroblasts. CAF-conditioned medium enhanced EJ-1 cell viability, migration, and Matrigel invasion; these effects were weakened by GLG1 silencing and strengthened by GLG1 overexpression in CAFs. In xenografts, CAFs-shGLG1 reduced tumor growth and Ki-67 positivity and increased TUNEL-positive tumor cells relative to CAFs-shNC, whereas CAFs-OE-GLG1 showed the opposite Ki-67 and TUNEL staining pattern. CAF-associated GLG1 promotes bladder cancer cell viability, migration, Matrigel invasion, and xenograft growth while limiting tumor-cell apoptosis, likely by reinforcing tumor-stromal crosstalk. These findings support GLG1 as a stromal factor involved in bladder cancer progression and provide a basis for further evaluation of its biomarker potential and therapeutic relevance. - Source: PubMed
Publication date: 2026/09/23
Liu JingpengZhou ZhongbaoZhang BainingLiu RunzeZhang Yong - Severe tuberculosis (STB) imposes a substantial disease burden, yet reliable biomarkers for distinguishing STB from mild/moderate tuberculosis (MTB) remain scarce. This study aimed to identify and independently validate plasma protein biomarkers associated with tuberculosis severity. - Source: PubMed
Publication date: 2026/09/14
Hu YifanXue YuShu WeiRen WeicongLi RuiMa ZichunLiu RuichaoPang YuLi Liang