HSP90AA1 Antibody - N-terminal region (P100674_P050)
- Known as:
- HSP90AA1 Antibody - N-terminal region (P100674_P050)
- Catalog number:
- p100674_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HSP90AA1 Antibody - N-terminal region (P100674_P050)
Related genes to: HSP90AA1 Antibody - N-terminal region (P100674_P050)
- 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: HSP90AA1 Antibody - N-terminal region (P100674_P050)
Related articles to: HSP90AA1 Antibody - N-terminal region (P100674_P050)
- Type 2 diabetes mellitus (T2DM) has emerged as a major global public health concern, characterized by increasing prevalence and serious complications that contribute substantially to societal healthcare costs. Concurrently, endoplasmic reticulum stress (ERS) has been increasingly appreciated as a central pathogenic mechanism underpinning the development and progression of T2DM. Calcitriol has been shown to have a beneficial effect in the treatment of T2DM. However, the therapeutic targets and potential mechanisms of calcitriol against T2DM through modulated ERS-related pathways remain poorly understood. To systematically investigate these mechanisms, we adopted an integrated approach combining network pharmacology, molecular docking and experimental validation. Initial network pharmacology analysis identified STAT3, HSP90AA1, MAPK1, and PIK3R1 as potential key targets mediating calcitriol's anti-T2DM effects. These computational predictions were then experimentally validated using a high glucose (HG)-induced MIN6 cell model. Functional assessments using CCK-8 assays and flow cytometry demonstrated that calcitriol improved the survival of pancreatic β-cells and reduced glucose-induced cell death. Moreover, the results from real-time fluorescent quantitative PCR and western blot analysis revealed that calcitriol reversed the HG induced upregulation of STAT3, HSP90AA1, MAPK1 and PIK3R1 mRNA and protein levels in MIN6 cells. The findings from our study may offer insights into the underlying mechanisms through which calcitriol exerts its therapeutic effects on T2DM by targeting potential ERS-related pathways. - Source: PubMed
Publication date: 2026/04/16
Zeng FanqiangLiao YimeiJiang JianpingZhao ChengjianPeng ShuihuaZhang HuijieZou HuiTan ShudanQiao LiyaLiu FanHuo JuanYan ZhigangXu Yongli - Thyroid cancer (THCA) is the most prevalent endocrine malignancy, underscoring the need for novel therapies. Pachymic acid (PA), a key bioactive triterpenoid from P. cocos, possesses documented anticancer activity, yet its role in thyroid cancer is poorly understood. In this study, we evaluated PA's effects on THCA in vitro and in vivo. Our results revealed that PA potently suppressed THCA cell proliferation, migration and tumor growth. Metabolite profiling identified seven metabolites and their formation pathways. Network pharmacology predicted 147 therapeutic targets, primarily enriched in PI3K-AKT, MAPK, and EGFR signaling, and PA was shown to exhibit the strong and stable binding affinity with AKT, EGFR, HSP90AA1, which was functionally validated by Western blot showing inhibition of AKT (Ser473) and EGFR (Tyr1068) phosphorylation. Crucially, hydrolytic metabolites M4-M7 exhibited superior binding affinity to AKT and EGFR. In summary, PA inhibits thyroid cancer cell proliferation likely through blocking AKT and EGFR signaling, and its hydrolytic metabolites M4-M7 may mediate enhance antitumor activity via more potent target engagement. - Source: PubMed
Publication date: 2026/04/13
Wang FengLi JingHu BinTang MengChen Jian - Dental caries is a significant global oral health problem, primarily caused by Streptococcus mutans (S. mutans). Although previous studies have indicated that Caesalpinia sappan (CS) exhibits anti-caries properties, its specific anti-caries active compounds remain largely unidentified. This study aimed to identify the potential anti-caries components of CS through an integrated strategy involving bioassay-guided isolation targeting S. mutans, UPLC-MS/MS, network pharmacology, molecular docking, and molecular dynamics simulation. Bioassay-guided isolation led to the identification of 33 compounds in fraction 5 from CS, among which brazilin showed the highest content and effectively inhibited biofilm formation and acid production by S. mutans. Network pharmacology analysis predicted 11 active ingredients in CS, including brazilin, targeting 7 potential targets related to dental caries: AKT1, EGFR, BCL2, PTGS2, MMP9, ERBB2, and HSP90AA1, as well as two pathways-nitrogen metabolism and calcium signaling. Molecular docking revealed strong binding affinities of brazilin to PTGS2, EGFR, MMP9, GtfC, GtfD, and GbpC. Further, molecular dynamics simulation revealed strong stability between brazilin and PTGS2, GtfC. Together, these findings not only clarify the anti-caries chemical constituents of CS and their potential mechanisms of action, but also provide new insights into the bioactive components and mechanisms of natural plant-derived medicines for the prevention and treatment of dental caries. - Source: PubMed
Publication date: 2026/04/14
Jia YongliangZhang DongdongLu HongxingLi YanhongWang Yuehu - Alpha-mangostin (AM), a xanthone from , has shown promising nephroprotective properties, but its mechanisms in acute kidney injury (AKI) remain incompletely defined. In this study, we applied an integrative network pharmacology pipeline combined with molecular docking to clarify AM's multi-target mechanisms in AKI. We identified 128 predicted AM targets and intersected them with AKI-related genes, yielding 122 shared targets. Protein-protein interaction analysis identified ten hub genes-, , , , , , , , , and -implicating inflammatory, hypoxia, and cell-survival pathways. KEGG enrichment highlighted HIF-1 signaling, PI3K-Akt signaling, chemokine signaling, AGE-RAGE signaling, and pathways related to cellular senescence and oxidative stress, while GO terms emphasized responses to chemical/oxygen-containing compounds, kinase activity, signal transduction, and apoptosis. Molecular docking against the ten hub proteins showed favorable binding energies across multiple targets. The strongest predicted affinities were observed for PTGS2 (-11.13 kcal/mol), TNF (-9.74 kcal/mol), and AKT1 (-9.48 kcal/mol). Docking positioned AM within the COX-2 catalytic pocket, engaging key catalytic and hydrophobic residues similar to known inhibitors. MD simulation interaction analysis confirmed that AM maintained stable contacts with key human PTGS2 residues, characterized by dominant hydrogen bonds and water-bridge interactions with SER353, TYR355, ARG513, and SER530, along with consistent hydrophobic contacts, and persistent interactions sustained throughout the 200 ns trajectory. Collectively, these results suggest that AM modulates interconnected inflammatory, hypoxic, and survival pathways relevant to AKI, acting as a multi-target ligand with notable interaction involving COX-2, TNF, and AKT1. Further experimental validation and formulation strategies to improve bioavailability are recommended for the advancement of AM toward therapeutic evaluation in AKI. - Source: PubMed
Publication date: 2026/04/07
Chatatikun MoragotTedasen AmanJansakun ChutimaPoolbua PassakornHuang Jason CThanasai JongkonneeKlangbud Wiyada KwanhianPhongphithakchai Atthaphong - Multiple myeloma (MM) is a hematologic malignancy commonly treated with bortezomib (BTZ). However, treatment efficacy is often limited by the development of BTZ resistance. Icaritin has demonstrated broad anti-tumor activities. This study aimed to investigate the effect of Icaritin on the malignant progression of MM and its potential to overcome BTZ resistance. The anti-MM activity of Icaritin was evaluated through a series of experimental approaches, including cell counting kit 8, flow cytometry, 5-ethynyl-2'-deoxyuridine, network pharmacology, molecule docking, reverse transcription-quantitative polymerase chain reaction, Co-Immunoprecipitation (CoIP), and western blot. Icaritin suppressed MM cell viability and proliferation, induced ferroptosis, and enhanced cellular sensitivity to BTZ. Moreover, Icaritin inhibited HSP90α family 1 (HSP90AA1) protein expression via promoting ubiquitination. HSP90AA1 facilitated MM cell proliferation, suppressed ferroptosis, and attenuated BTZ sensitivity. Notably, Icaritin promoted MM cell ferroptosis and BTZ sensitivity by inhibiting HSP90AA1. In vivo, Icaritin enhanced the sensitivity of tumor cells to BTZ. Icaritin suppresses malignant progression, induces ferroptosis, and enhances BTZ sensitivity in MM by inhibiting HSP90AA1. These findings provide a novel theoretical basis for Icaritin treatment of MM and regulation of BTZ sensitivity. - Source: PubMed
Shi LinLv DianliangWang XueyingZhang KuanshunFeng LeiZhang RunfangZhao Jiangshan