HSP90B1 Antibody
- Known as:
- HSP90B1 Antibody
- Catalog number:
- 51-108
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- HSP90B1 Antibody
Related genes to: HSP90B1 Antibody
- 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
Related products to: HSP90B1 Antibody
Related articles to: HSP90B1 Antibody
- 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 - Diabetic nephropathy (DN) has emerged as the leading cause of end-stage renal disease, with oxidative stress injury and excessive autophagy implicated in its pathogenesis. Elevated levels of the ITIH3 protein are considered closely associated with kidney-related diseases. However, the role of ITIH3 in the progression of DN remains unclear. By collecting peripheral blood from patients with DN, establishing a type 2 diabetic mouse model induced by streptozotocin (STZ), and exposing renal tubular epithelial cells (RTECs) to high glucose (HG) conditions, we comprehensively investigated the role of ITIH3 in DN at clinical, animal, and cellular levels. The ITIH3 level in DN patients' peripheral blood was elevated and positively correlated with inflammatory markers. At the cellular level, HG stimulation upregulated ITIH3 in RTECs, enhancing apoptosis, fibrosis, inflammation, oxidative stress, and autophagy, while silencing ITIH3 suppressed these damages. Molecularly, silencing ITIH3 upregulated HSP90B1, increased STAT3 ubiquitination, and inhibited its activation; silencing HSP90B1 reversed ITIH3-silencing's benefits, and overexpressing STAT3 counteracted HSP90B1-overexpression's effects. At the animal level, DN mice showed elevated blood glucose, renal hypertrophy, impaired function, and increased fibrosis, inflammation, and autophagy, whereas ITIH3 silencing reduced blood glucose and alleviated these abnormalities. Our research findings reveal that silencing ITIH3 up-regulates HSP90B1, which in turn elevates the ubiquitination level of STAT3 and suppresses its activation. This, consequently, inhibits oxidative stress and autophagy in RTECs. These results offer a promising therapeutic approach for the treatment of DN. - Source: PubMed
Publication date: 2026/09/12
Deng WeiJiang JialinLin MiaoLin WeiChen GangLi YukunWen Junping - This study examined the mechanisms underlying the comorbidity between type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease (ASCVD), while identifying potential therapeutic targets. Common differentially expressed genes (C-DEGs) between T2DM and ASCVD were extracted from the GSE78721 and GSE12288 datasets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, protein-protein interaction (PPI) network construction, hub gene identification, and Drug-Gene Interaction Database (DGIdb) analysis were conducted. The association between hub C-DEGs and immune-infiltrating cells was analyzed using the CIBERSORT method. Expression levels of hub C-DEGs were quantified through qRT-PCR and Western blot analyses. A total of 32 C-DEGs were identified, comprising 20 upregulated and 12 downregulated genes. C-DEGs were predominantly enriched in key pathways, including viral myocarditis, arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy, and dilated cardiomyopathy. PPI analysis revealed 29 nodes and 39 edges, leading to the identification of eight hub C-DEGs (HSP90B1, PLAU, SLPI, TOP3A, NCF4, PRF1, TUBA1C, and CS) across both datasets. Furthermore, hub C-DEGs (TOP3A, SLPI, NCF4, PRF1, and PLAU) demonstrated significant correlations with immune-infiltrating cell levels. Drugs specifically targeting these hub C-DEGs present promising candidates for the treatment of T2DM and ASCVD. Additionally, the expression of hub C-DEGs at both mRNA and protein levels was validated in patients with T2DM and ASCVD. An integrated bioinformatics analysis facilitated the screening of candidate therapeutic targets, mechanisms, and drugs for T2DM and ASCVD, offering new insights into molecular therapies for these conditions. - Source: PubMed
Publication date: 2026/08/04
Du WeiMa GuiyingLi BingGong FanZhang Yun - A strong crosstalk exists between endoplasmic reticulum (ER) stress and synovitis. Beyond their canonical role in protein folding, ER stress chaperones may promote inflammation, cell survival, and fibroblast activation under pathological conditions. This study aimed at localizing and quantifying 11 ER stress proteins (BiP, HYOU1, MANF, PDIA4, GANAB, HSP90B1, TXNDC5, DNAJB11, LMAN1, ERP29, CALR) in human inflamed synovial membranes and at investigating their expression in fibroblast-like synoviocytes (FLS) under ER stress, pro-inflammatory, or pro-fibrotic stimuli. By immunohistochemistry, on a first cohort of formalin-fixed paraffin-embedded (FFPE) biopsies obtained from patients with osteoarthritis (OA), chronic pyrophosphate arthropathy (CPPA), and rheumatoid arthritis (RA), these ER chaperones were primarily localized to the lining in low-grade inflammation (Tak <4) and expanded to the sublining under high inflammatory conditions (Tak ≥4), with a widespread distribution in RA. Imaging mass cytometry, applied to a second cohort of FFPE tissue samples collected from patients diagnosed with OA and RA, revealed the co-expression of ER stress proteins with CD55⁺ FLS in the lining and their progressive infiltration into the sublining along with CD34⁺CD31 FLS during inflammation. These observations were confirmed by immunofluorescence on a larger cohort of OA patients. As inflammation progresses, there is a loss of co-expression with CD55 in the lining, accompanied by a gradual shift towards co-expression with CD34 in the sublining. In vitro, ER stress proteins, particularly BiP, HYOU1, MANF, PDIA4, HSP90B1, LMAN1, CALR, and DNAJB11 are overexpressed in human OA FLS following ER stress, pro-inflammatory or pro-fibrotic stimulation, with BiP, PDIA4, HSP90B1, ERP29, and CALR also being secreted. PDIA4 emerged as a central player: its depletion significantly impaired FLS proliferation and migration, highlighting a direct role in driving synovitis. This study provides the first spatial and functional characterization of ER chaperones in human arthritic synovium, linking ER stress to fibroblast plasticity, inflammation, and fibrosis. - Source: PubMed
Publication date: 2026/08/12
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