Hsp90 Polyclonal Antibody
- Known as:
- Hsp90 Polyclonal Antibody
- Catalog number:
- ASASPA-846D
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Hsp90 Polyclonal Antibody
Related genes to: Hsp90 Polyclonal Antibody
- 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 Polyclonal Antibody
Related articles to: Hsp90 Polyclonal Antibody
- Tropical heat and humidity induce oxidative and thermal stress that threaten male fertility. However, the seminal plasma mechanisms that sustain sperm function under these conditions in goats remain poorly understood. - Source: PubMed
Publication date: 2026/01/31
Damayanti ErniDiansyah Athhar ManabiAzis Ismah UlfiyahIrawan FahrulMaulana TulusMuhajir MasturiDagong Muhammad Ihsan AndiKartika Nur Amalia - As a common anesthetic, Sevoflurane may be involved in the development of postoperative cognitive dysfunction (POCD) in the elderly. This study aims to investigate whether Sevoflurane regulates mitophagy in hippocampal neurons in elderly POCD through HSP90AA1, using a network pharmacology-based approach. Multiple databases were used to screen the common targets of Sevoflurane, mitophagy and elderly POCD, and GO and KEGG pathway enrichment analyses were performed. The protein-protein interaction network was constructed using STRING database and Cytoscape software, and the binding characteristics of Sevoflurane to the core target HSP90AA1 were verified by molecular docking and dynamics simulation. For cellular experiments, mouse hippocampal neuronal cells (HT22) were treated with Sevoflurane, and rescue experiments were performed by knocking down HSP90AA1 (sh-HSP90AA1). Cell viability, oxidative stress, mitochondrial membrane potential (MMP), the expression of mitophagy markers and cell apoptosis were evaluated by CCK8 assay, LDH release detection, ROS detection, JC-1 staining, western blot and flow cytometry. A total of 42 common targets of Sevoflurane, mitophagy and elderly POCD were screened, among which HSP90AA1 was identified as one of the key hub targets. Molecular docking showed that Sevoflurane had a stable binding ability with HSP90AA1. Cell experiments showed that Sevoflurane treatment significantly inhibited HT22 cell viability and p63 protein expression, while increased LDH release, ROS level, MMP depolarization, LC3-II/LC3-I, PINK1, Parkin, HSP90AA1 protein expression, and cell apoptosis. However, knockdown of HSP90AA1 reversed the above cell injury effects induced by Sevoflurane. Sevoflurane may promote oxidative stress, mitophagy and apoptosis of hippocampal neurons by upregulating HSP90AA1, thereby aggravating the process of POCD in the elderly. These results suggest that HSP90AA1 is a potential key target for Sevoflurane-mediated neuronal injury. - Source: PubMed
Publication date: 2026/06/29
Liu XiuFengZhang ChenLiu Juan - This study aims to elucidate the mechanisms underlying bisphenols (BPs)-induced neurodegeneration and their contribution to neurodegenerative diseases. Focusing on four major disorders-Alzheimer's Disease, Parkinson's Disease, Amyotrophic Lateral Sclerosis, and Huntington's Disease-we systematically examined key molecular pathways potentially perturbed by BPs during disease progression. Preliminary toxicological profiling of four representative BPs was conducted using ProTox-3.0, ADMETlab 3.0, and the Xundrug database. Subsequent target identification involved integrated analyses of multiple bioinformatics resources, including CHEMBL and STITCH. Protein-protein interaction networks constructed with STRING and Cytoscape identified core targets such as HSP90AA1, ESR1, BCL2, and PTGS2. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses further revealed critical biological processes, including enzyme binding and heme binding, as well as key pathways associated with BPs neurotoxicity, such as chemical carcinogenesis-receptor activation, chemical carcinogenesis-DNA adducts, and arachidonic acid metabolism. Molecular docking studies demonstrated strong binding affinities between BPs and core targets, supported by low free energy values. Molecular dynamics simulations further validated stable binding conformations and dynamic interactions. Additionally, we analyzed regulatory networks of mRNA-miRNA-lncRNA interactions for core targets. In summary, our findings establish a novel multi-target and multi-pathway framework for BPs-induced neurodegeneration, revealing synergistic effects of pathways including carcinogenic signaling activation and metabolic dysregulation. This study advances understanding of environmental neurotoxicity and provides a foundation for developing preventive strategies against neurodegenerative diseases. - Source: PubMed
Publication date: 2025/08/19
Liu HuiTang MengyaoChe LuqiaoLu JianingZhang Liping - We applied the TempO-LINC® platform to generate single-cell transcriptomic (SCTr) profiles of ∼40,000 HepaRG cells exposed to etoposide, brefeldin A, cycloheximide, rotenone, tBHQ, troglitazone, and tunicamycin at three concentrations for 24 hours. SCTr enabled a detailed analysis of adaptive stress response pathways (SRPs), including the unfolded protein response (UPR), oxidative stress response (OSR), heat shock response (HSR), and DNA damage response (DDR). Troglitazone upregulated lipid metabolism genes () along with HSR and UPR activation, with co-expression of , and in subsets of cells. Brefeldin A and tunicamycin strongly induced UPR markers () in subsets of cells, with some also expressing apoptotic () and autophagic () genes, indicating diverse stress responses. Rotenone activated , and in a fraction of cells, accompanied by and mild UPR induction, reflecting heterogeneous mitochondrial stress responses. We scored individual cells using literature-derived SRP gene signatures to characterize overall stress phenotypes and clustered them using a generalized Jaccard metric. The clustering revealed five phenotypic groups spanning cell states associated with homeostasis, adaptive responses, terminal outcomes, autophagy, and apoptosis. By systematically analyzing the distributions of cells in different states across treatments, we visualized dynamic shifts in cellular subpopulations responding to chemicals, revealing early stress responses and potential transitions to cell death. Our findings suggest the utility of SCTr in decoding stress states that could provide possible insights into transitions between cellular adaptive and terminal transitions involved in toxicity. - Source: PubMed
Publication date: 2025/08/26
Shah ImranGallegos DavidRobinette BrianChambers Bryant AEastburn Dennis JBell Douglas ACampbell Michelle RMartos Suzanne NCamiolo SalvatoreWhite Kevin SMartin NicoleMontis GioeleMcComb JoelSeligmann BruceChorley Brian N - Liver hepatocellular carcinoma (LIHC) remains a critical health challenge with limited treatments. This study employed network toxicology and molecular docking to investigate how polycyclic aromatic hydrocarbons (PAHs), as environmental carcinogens, promote LIHC. By analyzing TCGA LIHC data and screening genes via the Comparative Toxicogenomics Database, 1,817 key PAH-LIHC-related genes were identified. Enrichment analyses revealed associated biological pathways, and a protein-protein interaction network pinpointed 321 MCODE-derived functional module genes. A prognostic risk model based on 14 model genes was developed, demonstrating high accuracy in predicting 1 year survival for LIHC patients. Immune infiltration analysis showed distinct profiles between high- and low-risk groups. Molecular docking showed favorable docking scores and potential binding conformations of PAHs to key genes (ANXA5, LOX, HSP90AA1). Among these, the ANXA5-805-PAH complex was further subjected to a 50 ns molecular dynamics simulation to describe its short-term dynamic behavior. The results provide exploratory computational clues for PAH-related candidate targets, but further confirmation is required through rigorous docking protocol validation, repeated simulations, and experimental studies. This research provides a PAH-related prognostic model and elucidates molecular mechanisms of environmental toxin-driven liver cancer. - Source: PubMed
Publication date: 2026/06/28
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