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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- 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
Gendebien ZoéPoulet ChristopheDeroyer CélinePaulissen GenevièveSalpetier PaulineHego AlexandreLefèvre GaëtanCobraiville GaëlNeuville SophiePlener ZeldaDaniel ChristopheThirion ThierrySokolova TatianaDurez PatrickHemon PatriceDelarue YunaMarec NadègeBianchi ElettraDelvenne PhilippeRibbens Cliode Seny Dominique - Deer antler is the only mammalian organ capable of periodic complete regeneration. Its astonishing growth rate-reaching several centimeters per day-provides a unique model for research in tissue regeneration and developmental biology. This rapid growth relies on the protective and signaling functions of the skin, as well as the vigorous proliferation and differentiation capacity of mesenchymal cells. Although previous studies have identified some key factors involved in antler growth, systematically comparing the transcriptomic profiles of these two core tissues (skin and mesenchyme) to identify candidate genes regulating their synergistic growth is crucial for deciphering the molecular mechanisms underlying this "ultra-fast" growth. - Source: PubMed
Publication date: 2026/07/27
Bi XiaodanLiu BingLi BingZhao MeirongTian HuiminChen Jianxing - Poricoic acid A (PAA) is a bioactive triterpenoid from the fungus Poria cocos. Nevertheless, whether it exerts antidepressant-like effects and whether the gut microbiota and immune regulation are involved remain unknown. - Source: PubMed
Publication date: 2026/07/30
Yang JiangweiMa YunLiang ZixinWang ShuihongWang Heqiu - The Notch receptor, GLP-1 , is essential for germline proliferation and early embryonic development. While the cytosolic chaperone HSP-90 promotes GLP-1 signaling in the germline, it is unknown whether the endoplasmic reticulum-resident Hsp90, ENPL-1 (GRP94/endoplasmin), also promotes GLP-1 signaling. We used RNAi knockdown of in a sensitized background to investigate potential genetic interactions. RNAi-mediated knockdown of did not enhance reduced GLP-1 /Notch signaling, and it caused a similar degree of early larval arrest in both wildtype and backgrounds. Thus, we did not detect a role for ENPL-1 in promoting GLP-1 /Notch signaling. - Source: PubMed
Publication date: 2026/07/08
Lissemore James LPancake AmandaFang ShurongMaine Eleanor M