Hsp90 Mab (16F1), Biotin Conjugate
- Known as:
- Hsp90 Mab (16F1), Biotin Conjugate
- Catalog number:
- ASASPA-835BE
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Hsp90 Mab (16F1) Biotin Conjugate
Related genes to: Hsp90 Mab (16F1), Biotin Conjugate
- Gene:
- HSP90AA1 NIH gene
- Name:
- heat shock protein 90 alpha family class A member 1
- Previous symbol:
- HSPC1, HSPCA
- Synonyms:
- Hsp89, Hsp90, FLJ31884, HSP90N
- Chromosome:
- 14q32.31
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-27
- Date modifiied:
- 2016-10-11
Related products to: Hsp90 Mab (16F1), Biotin Conjugate
Related articles to: Hsp90 Mab (16F1), Biotin Conjugate
- Allergic rhinitis (AR) is one of the most prevalent allergic disorders worldwide. Current pharmacological treatments are often limited by suboptimal efficacy and notable adverse effects. Herbal medicines, with their multi-component and multi-target therapeutic characteristics, have attracted increasing attention. Krasch. (AOK), a traditional Chinese/Mongolian medicine has demonstrated immunomodulatory, antioxidant, and anti-inflammatory activities. The anti-AR potential of AOK extract fractions was evaluated using in vitro mast cell degranulation inhibition assays, network pharmacology analysis, molecular docking, and molecular dynamics simulations to elucidate underlying pharmacological mechanisms. The P815 mast cell model induced by compound 48/80 was employed to assess the inhibitory activity and cytotoxicity of different extract fractions. Among the tested fractions, the ethyl acetate fraction exhibited the most potent inhibitory effect on mast cell degranulation without significant cytotoxicity. Network pharmacology analysis identified 254 potential AR-related targets of AOK, with Signal Transducer and Activator of Transcription 3(STAT3), Src protein(SRC), Tumor protein 53(TP53), AKT Serine/Threonine Kinase 1(AKT1), Heat Shock Protein 90 Alpha Family Class A Member 1(HSP90AA1), Estrogen Receptor 1(ESR1), and Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha(PIK3CA) identified as key hub proteins. Gene Ontology and KEGG pathway enrichment analyses indicated that AOK primarily modulated inflammatory and oxidative stress-related processes through the lipid and atherosclerosis, hypoxia-inducible factor-1, and AGE-RAGE signaling pathways. Molecular docking and dynamics simulations demonstrated strong binding affinities and stable interactions between major active constituents, particularly hydroxygenkwanin, and key targets such as SRC. The ethyl acetate fraction of AOK extract exhibited significant mast cell degranulation inhibitory activity, likely mediated via a synergistic multi-component, multi-target mechanism involving regulation of inflammatory and immune-related signaling pathways. These findings provide a pharmacological basis for the potential application of AOK in AR treatment. - Source: PubMed
Publication date: 2026/06/05
Wang MengmengZou JingmingZhang QiBai XianxiangWu SiHu YaweiHan XiaoyanHan NaXiao Bin - Cadmium(Cd) exposure is associated with anxiety, but mechanism-informed multi-target interventions are limited. - Source: PubMed
Publication date: 2026/05/25
Tian MaoqinWan ShengGao HaoYin YinghuiHan FengYang YongLiu ZhenzhongZhao QihanHuang Shaoxin - Insomnia is closely associated with immune dysregulation, yet the overall pattern of peripheral-central immune disequilibrium and its underlying molecular basis remains incompletely understood. To characterize the peripheral-central immune features associated with insomnia, identify key immune cell populations and core molecular programs, and prioritize candidate therapeutic compounds with preliminary experimental validation. Peripheral blood bulk transcriptomic dataset GSE208668 was analyzed using differential expression analysis, weighted gene co-expression network analysis (WGCNA), and functional enrichment analysis to identify insomnia-associated genes. Protein-protein interaction network analysis and machine learning models were then applied in independent peripheral blood datasets to refine core genes. Immune deconvolution and peripheral blood single-cell transcriptomic dataset GSE213496 were used to determine the immune-cell context, cell-type localization, and intercellular communication features of these genes. The brain single-cell transcriptomic dataset GSE137665 was further analyzed to assess central alterations. Drug prediction, molecular docking, and molecular dynamics simulations were performed to prioritize candidate compounds, followed by in vitro validation of resveratrol in an LPS-induced THP-1 macrophage model. A total of 5,321 differentially expressed genes associated with insomnia were identified, and weighted gene co-expression network analysis highlighted the turquoise and blue modules as key insomnia-related modules. Integrative analysis yielded 390 intersecting genes enriched mainly in immune, inflammatory, and oxidative stress-related pathways. Protein interaction analysis and machine learning further identified six refined core genes: FN1, HMOX1, HSP90AA1, IL10, MYD88, and NFE2L2. Because IL10 was not stably detected in the single-cell datasets, the remaining five genes were used for downstream single-cell analyses. Immune deconvolution suggested selective peripheral immune remodeling in insomnia, characterized by increased resting CD4 memory T cells and M2 macrophages, together with reduced activated NK cells. Peripheral single-cell analysis showed that HMOX1, HSP90AA1, MYD88, and NFE2L2 were mainly enriched in neutrophils, inflammatory macrophages, conventional dendritic cells, and selected lymphocyte populations, whereas FN1 showed a more restricted distribution pattern. CellChat analysis indicated enhanced intercellular communication under the sleep deprivation-related condition. In contrast, brain single-cell analysis revealed comparatively modest but detectable central alterations, including enrichment of ependymal cells, slight increases in excitatory neurons, brain endothelial cells, and choroid plexus stromal fibroblasts, together with heterogeneous expression of the core hub genes and selective rewiring of intracerebral communication networks. Drug prediction consistently prioritized quercetin and resveratrol, and structural analyses supported stable interactions with key targets. In THP-1 macrophages, resveratrol downregulated MYD88 and HSP90AA1 while further upregulating HMOX1. Insomnia appears to be associated predominantly with a peripheral-centered immune disequilibrium pattern, characterized by selective remodeling of innate immune-related populations, enhanced inflammatory and oxidative stress programs, and increased intercellular communication. The MYD88-HMOX1-HSP90AA1-NFE2L2 axis may represent a key molecular program linking inflammatory activation and oxidative stress adaptation. Resveratrol was identified as a potential compound and has been validated through preliminary in vitro experiments. - Source: PubMed
Publication date: 2026/06/10
Zhu WenwenWen ZhijuanGao YimengHe BijuanChen RuitongPan HaosenBin WeiYang ZhiminTan Fei - Respiratory syncytial virus (RSV), a single-stranded negative-sense RNA virus, is a major pathogen of acute respiratory tract infections, posing severe threats to the health of infants, the elderly and immunocompromised individuals. While approved vaccines for older adults and monoclonal antibody prophylaxis for infants are available, effective therapeutic drugs remain scarce. Resveratrol, a phenolic compound naturally present in grapes, berries and other foods, has been confirmed to exhibit anti-RSV activity, but its molecular mechanism of action remains unclear. - Source: PubMed
Xia JianboShi ZuliangShen Mengxin - Polyhexamethylene guanidine phosphate (PHMG-p), a cationic disinfectant previously used in humidifiers, has been linked to severe pulmonary diseases in Korea. This study aimed to elucidate the molecular mechanisms underlying PHMG-p-induced lung toxicity using an integrated multi-omics approach. BALB/c mice were intratracheally instilled with PHMG-p (0, 0.03, 0.1 mg/kg, twice weekly for 4 weeks). Histopathology revealed dose-dependent pulmonary lesions, including inflammatory infiltration, alveolar wall hyperplasia, and fibrosis. Transcriptomic profiling identified 213 and 1,506 differentially expressed genes (DEGs) in the low- and high-dose groups, respectively, with enriched pathways related to immune activation, cytokine signaling, and cellular stress responses. Proteomic analysis detected 148 and 1,168 differentially expressed proteins (DEPs), many of which overlapped with DEGs and were associated with chemokine signaling, protein refolding, and ion transport dysregulation. Metabolomic profiling of serum samples identified dose-responsive alterations in amino acid and energy metabolism, with notable increases in glutamate, leucine, serine, and related metabolites. Integrated omics analysis revealed consistent up-regulation of CDKN1A, HSP90AA1, HSPA1A, HSPA8, and HSPH1, and down-regulation of FPR1, suggesting their roles as potential biomarkers of PHMG-p-induced pulmonary injury. Pathway convergence indicated activation of inflammatory and fibrotic remodeling processes, as well as metabolic reprogramming involving glutamate and branched-chain amino acid pathways. These findings provide mechanistic insight into PHMG-p-induced lung toxicity and highlight multi-omics signatures that may serve as biomarkers for monitoring or predicting pulmonary damage caused by cationic polymer biocides. - Source: PubMed
Publication date: 2026/06/08
Lee Jung DaeKim Hyang YeonIm Jueng-EunLee HandulePark JuyoungPark KwangsikKang KeunsooJeong Hye GwangChae SehyunHwang DaeheeHan Beom SeokCho Wan-SeobKim SuhkmannKim Kyu-Bong