Hsp90 Antibody Sample Pack
- Known as:
- Hsp90 Antibody Sample Pack
- Catalog number:
- ASAPAK-010
- Product Quantity:
- 8 x 25 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Hsp90 Antibody Sample Pack
Related genes to: Hsp90 Antibody Sample Pack
- 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 Antibody Sample Pack
Related articles to: Hsp90 Antibody Sample Pack
- Aflatoxins are widespread dietary contaminants with potent carcinogenicity, yet the molecular mechanisms of most congeners beyond AFB1 remain poorly characterized. To systematically elucidate the carcinogenic targets and mechanisms of five dietary aflatoxins-AFB1, AFB2, AFG1, AFG2, and AFM1-through network toxicology, pan-cancer analysis, and molecular docking. Toxicity was predicted using ProTox-3.0. Potential targets were identified from multiple databases, followed by GO and KEGG enrichment analyses. PPI networks were constructed, and core genes were identified using six topological algorithms. Pan-cancer expression, mutation, and survival were analyzed using TCGA and GTEx data. Immune infiltration, single-cell functional analyses, and molecular simulation were performed. All five aflatoxins were active carcinogens (0.59-0.68). Fifty-one common targets were identified, enriched in GPCR signaling and neurotransmitter pathways. Cross-analysis with cancer genes yielded 23 overlapping genes, with PTGS2, PIK3CA, and HSP90AA1 as core targets. These genes were differentially expressed across multiple cancers and associated with survival. PIK3CA showed the highest mutation frequency (89%). Immune infiltration revealed negative correlations with CD8 + T cells and positive with Tregs. Molecular simulation confirmed effective potential binding. PTGS2, PIK3CA, and HSP90AA1 are core carcinogenic targets of dietary aflatoxins, demonstrating that multiple congeners share common carcinogenic pathways with implications for food safety risk assessment. - Source: PubMed
Publication date: 2026/07/17
Lin PengCheng WeiQi XinLi Jing - Periodontitis, driven by () biofilms, is a global health burden with limited treatment options due to antibiotic resistance. is traditionally used in China for clearing heat and reducing swelling, yet its anti-periodontitis potential remains uncharacterized. This study evaluated the antibacterial and therapeutic effects of its essential oil (CLEO) against periodontitis. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of CLEO against were determined by broth microdilution. Anti-biofilm activity was assessed via XTT assay. Network pharmacology, molecular docking, and 100 ns molecular dynamics simulations were employed to identify active compounds and core targets. Experimental periodontitis was induced in C57BL/6 mice by molar ligation. Mice received topical CLEO at concentrations of 2, 3, and 4 mg/mL, 2% minocycline, or vehicle once daily for 14 days. Periodontal inflammation, alveolar bone loss, collagen organization, osteoclast activity, and serum levels of MMP-9 and COX-2 were evaluated. CLEO exhibited potent anti- activity, with an MIC of 2 mg/mL and MBC of 4 mg/mL. At the MIC, CLEO disrupted 57.5% of pre-formed biofilms. Network pharmacology and molecular docking identified α-bisabolol, chamazulene, and 1,8-cineole as key active compounds, with the chamazulene-HSP90AA1 complex showing the strongest binding affinity (-10.0 kcal/mol). The 100 ns MD simulation confirmed the stability of this complex (RMSD < 1 nm). In the mouse periodontitis model, topical application of CLEO at 3 and 4 mg/mL significantly reduced gingival inflammation, alveolar bone resorption, and the number of TRAP-positive osteoclasts compared with the vehicle-treated periodontitis group (all < 0.05). Furthermore, CLEO treatment dose-dependently lowered serum MMP-9 levels (from 24.15 ± 0.24 pg/mL in the model group to 12.36 ± 0.54 pg/mL in the high-dose group) and COX-2 levels (from 15.38 ± 0.62 pg/mL to 8.99 ± 0.57 pg/mL). The therapeutic efficacy of the high-dose CLEO group was comparable to that of the 2% minocycline group. CLEO exerts anti- and anti-biofilm effects in vitro and ameliorates periodontitis in vivo through multi-target mechanisms, providing pharmacological evidence for its traditional use in inflammatory conditions. - Source: PubMed
Publication date: 2026/07/02
Ma JuanLiu LikuanRen YiWang MingjinLi XingLi Jinping - Neutrophil extracellular traps (NETs) might be promising targets for the evaluation and treatment of pulmonary hypertension. However, no study has systematically screened NETs as feature genes and therapeutic targets in pulmonary hypertension. The present study aims precisely to address this issue. - Source: PubMed
Publication date: 2026/05/14
Li FangweiMa XiaohongLi RuxuanLi BinbinZhang Qi - Cancer remains a major global health challenge, demanding the development of novel and mechanism-based therapeutic strategies. In the present study, an integrated computational approach involving network pharmacology, molecular docking, ADMET profiling, and molecular dynamics simulations was employed to investigate the anticancer potential of bioactive compounds derived from the mushroom . Nine compounds with favourable predicted pharmacokinetic and toxicological properties were identified, yielding 138 potential cancer-related targets. Protein-protein interactions (PPIs) network analysis revealed 15 key hub genes, including CASP3, EGFR, ESR1, HSP90AA1, PPARG, MDM2, PARP1, SRC, PIK3CA, RELA, JAK2, PTGS2, GSK3B, PIK3R1, and TLR4, which are associated with several cancer types such as breast, colorectal, liver, and lung cancers. Functional enrichment analysis indicated the involvement of these targets in multiple cancer-related signaling pathways. Among these hub genes, EGFR emerged as a central therapeutic target due to its high network connectivity and involvement in multiple cancer-associated signaling pathways related to proliferation, survival, metastasis, and therapeutic resistance. Its prominent position within the interaction network further supports its potential as a key target for anticancer intervention. Molecular docking analysis demonstrated that lovastatin showed a strong predicted binding affinity toward EGFR, suggesting possible inhibitory potential. Molecular dynamics simulations further supported the stability of the lovastatin-EGFR complex. In addition, ADMET analysis indicated favourable drug-likeness and safety-related properties for the selected compounds. Overall, this study provides a systems-level computational investigation of -derived compounds and their potential interactions with cancer-associated targets. However, these findings are based on computational predictions and require further experimental validation to confirm their biological and therapeutic relevance. - Source: PubMed
Publication date: 2026/07/11
Maurya SupriyaEhsan SabaChaudhary AnupriyaYadav ShivanandSingh Mohan P - Systemic lupus erythematosus (SLE) is a highly heterogeneous autoimmune disease characterized by persistent immune activation and multi-organ damage. In this study, we integrated network pharmacology, molecular docking, and in vitro validation to identify and prioritize the active compounds, targets, and regulatory pathways of Artemisia argyi (AA). We identified nine candidate active compounds of AA and 380 predicted protein targets. Intersecting these with 218 SLE-associated genes yielded 19 overlapping targets, among which IL2, CASP3, ACE, PPARG, HSP90AA1, and ANXA5 exhibited the highest network connectivity. Functional enrichment analyses highlighted key pathways, including leukocyte activation, IL-17 signaling, and Th17 cell differentiation. Molecular docking revealed favorable binding affinities of quercetin and naringenin with several core targets. Among these, peroxisome proliferator-activated receptor gamma (PPARG) was selected for exploratory validation based on its high network centrality, favorable docking profile, characterized by strong binging affinities (<-5.5 kcal/mol) for both quercetin and naringenin. Subsequent bioinformatic screening identified LTF, CD72, IL13, CHI3L1, and TLR9 as putative SLE-associated genes regulated by PPARG. Experimentally, AA water extract (AAW) upregulated the expression of PPARG and these downstream genes in THP-1-derived macrophages, whereas pharmacological inhibition of PPARG significantly attenuated these effects. These findings suggest that AA modulate PPARG-dependent transcriptional signaling in immune cells, presenting a candidate mechanism that warrants further validation in disease-relevant models. - Source: PubMed
Publication date: 2026/07/10
Luo ManZhou XianleiYan ZimoZhang ZhiZhang Xuemei