Hsp90 Rabbit pAb
- Known as:
- Hsp90 Rabbit pAb
- Catalog number:
- ASASPA-836D
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Hsp90 Rabbit pAb
Related genes to: Hsp90 Rabbit pAb
- 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 Rabbit pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host RabbitExtraction-freeCE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host: Rabbit, Extraction-free, CE-marked Related articles to: Hsp90 Rabbit pAb
- BackgroundShort-chain organic acids (SCOAs) may have paradoxical effects on neurocognition, acting as either neuroprotective bioenergetic substrates or potential neurotoxicants. However, the joint effects of SCOA mixtures on cognitive impairment and the mechanisms underlying their divergent associations remain unclear.ObjectiveTo investigate the joint effects of serum SCOAs mixtures on cognitive impairment and elucidate underlying mechanisms.MethodsSerum levels of 11 SCOAs were quantified in 4192 older adults. Logistic regression and Bayesian kernel machine regression (BKMR) were used to assess individual and mixture associations with cognitive impairment. Potential targets were screened from public databases, intersected with cognitive impairment-related genes, and mapped to protein-protein interaction networks. Core targets were validated using four machine learning algorithms. Functional enrichment and molecular docking analyses were performed to explore potential mechanisms.ResultsIn adjusted models, β-hydroxybutyric, butyric, and propionic acids were inversely associated with cognitive impairment, whereas isobutyric and crotonic acids were positively associated. BKMR revealed a non-linear joint effect, with the overall association shifting from positive to negative when the mixture quantile exceeded 0.5; butyric acid showed an inverted U-shaped relationship. Network analysis identified two functional groups: the inverse group centered on GAPDH, AKT1, CASP3, NFKB1, and STAT3 and was enriched in PI3K-Akt and insulin signaling, whereas the positive group centered on ribosomal proteins and HSP90AA1, implicating ribosomal stress and NOD-like receptor signaling.ConclusionsSerum SCOAs showed divergent associations with cognitive impairment. Bioenergetic metabolites were linked to putative neuroprotective signaling, whereas risk-associated metabolites were linked to ribosomal stress signatures. - Source: PubMed
Publication date: 2026/07/28
Zhang ShuaiTao KequnZhou LuolinWang ShengGao ZhaoxingLiu XuGao LiRuan LiangXu YuanyuanLiu XuechunSong WeiTao FangbiaoLiu Kaiyong - Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS), differ in etiology but share several convergent pathological mechanisms. Pterostilbene (PTR) is a natural stilbene with reported antioxidant, anti-inflammatory, and neuroprotective properties. This study aimed to prioritize putative PTR-associated targets and biological processes potentially relevant to shared neurodegenerative mechanisms. An integrative in silico workflow combining network pharmacology, protein-protein interaction (PPI) analysis, GO Biological Process (GO BP) enrichment, molecular docking, and molecular dynamics (MD) simulations was applied. GO BP terms were filtered, focused on neurodegeneration- and neuroprotection-related processes, and subjected to REVIGO-based redundancy reduction. Selected targets were further evaluated by docking and 500 ns MD simulations. A total of 181, 165, 128, and 109 shared PTR-disease targets were identified for AD, PD, HD, and ALS, respectively. Redundancy-reduced GO BP analysis indicated associations with neuroinflammation, oxidative stress and reactive oxygen species-related responses, programmed cell death, MAPK/ERK- and PI3K/AKT-related signaling, ion and calcium transport, and lipid-, steroid-, or hormone-associated regulation. PPI topology prioritized SRC, ESR1, and HSP90AA1 as recurrent hub-bottleneck proteins, whereas MD-based structural interpretation focused on ESR1 and HSP90AA1. MD analyses indicated stable PTR interactions with both proteins, with ESR1 showing the most favorable predicted interaction profile. These findings suggest that PTR may interact with shared neurodegeneration-relevant molecular systems, particularly through ESR1- and HSP90AA1-associated mechanisms. However, the results are exclusively computational and should be interpreted as hypothesis-generating, requiring further experimental validation. - Source: PubMed
Publication date: 2026/07/08
Rosiak NataliaStojceski FilipMaroni GabrielePiontek BartoszCielecka-Piontek Judyta - This study aimed to use quantitative phosphoproteomics to explore phosphorylation characteristics in ()-induced liver abscess (KPLA) formation and liver injury. The strain LA- was phenotypically and genotypically characterized. A murine model of KPLA was established via intragastric inoculation. Phosphoproteomics and bioinformatic analyses were conducted to identify and quantify phosphosites and phosphoproteins. LA- displayed a hypermucoviscous phenotype, serotype K1, ST23 genotype, and harbored six major virulence genes. Inoculation induced liver colonization and typical histopathological abscess lesions. We quantified 3017 phosphoproteins covering 12,798 phosphosites (dominated by serine phosphorylation); 1723 proteins were upregulated and 425 downregulated. Bioinformatic analyses revealed remodeling in metabolism, stress response, signal transduction, and cytoskeleton organization. Upregulated proteins converged on fatty acid elongation, inositol phosphate metabolism, and the tricarboxylic acid cycle; downregulated proteins were enriched in PI3K-Akt, IL-17 signaling, and T-cell differentiation. Protein-protein interaction network analysis identified 10 key proteins (Src, Rac1, Actb, Hsp90aa1, Hsp90ab1, Egfr, Rps6, Pik3CA, Itgb1, and Fyn) that mediate inflammatory signaling, cytoskeleton remodeling, and immune infiltration. Dysregulated phosphorylation networks drive pathological metabolic adaptation, suppressed immune homeostasis, and cytoskeletal disorganization, collectively facilitating KPLA progression. The identified hub proteins and pathways represent high-value mechanistic targets and candidate therapeutic vulnerabilities for KPLA. - Source: PubMed
Publication date: 2026/07/14
Yan ChaoLiu XuanfengChen YujieSu AnRen XueZhang TingtingYuan Jing - Bisphenol A (BPA) is a potential risk factor for pancreatic ductal adenocarcinoma (PDAC). This study integrated network toxicology, molecular docking, molecular dynamics (MD) simulations, and TCGA clinical data analysis to explore the potential molecular mechanisms linking BPA exposure to PDAC risk. BPA-PDAC intersection targets were identified through multi-database screening, followed by protein-protein interaction (PPI) network construction to screen core hub genes. A total of 10 core hub genes were identified via PPI analysis combined with the Maximal Clique Centrality (MCC) algorithm. Molecular docking demonstrated that ESR1 exhibited one of the strongest binding affinities for BPA (-8.2 kcal/mol), and MD simulations confirmed favorable thermodynamic stability of the BPA-ESR1 complex. TCGA analysis revealed stage-dependent expression patterns: early stages showed downregulation of TP53 and BCL2, whereas advanced stages showed upregulation of BCL2L1, HSP90AA1, and HSP90AB1, while ESR1, HIF1A, and PARP1 remained consistently low. These findings suggest that BPA may promote PDAC progression by disrupting ERα-mediated endocrine signaling and impairing DNA repair through PARP1 interference, providing candidate molecular targets and a hypothesis-generating foundation for pancreatic cancer risk assessment, warranting further experimental validation. - Source: PubMed
Publication date: 2026/07/20
Li XueruWu FanZhang ZunhanAn JiayiZhou GuoqiangWang YangZhao DandanChen Xiaolu - Heart failure with preserved ejection fraction (HFpEF) is an increasingly common form of heart failure (HF) that is best understood as a systemic, multiorgan syndrome rather than a disease of left-ventricular filling alone. This review has three specific aims: first, to synthesize genetic and molecular pathways that are most relevant to non-ischemic HFpEF; second, to distinguish HFpEF-enriched mechanisms from evidence extrapolated from ischemic cardiomyopathy or HFrEF; and third, to consider translational implications for populations with high consanguinity, including the Kingdom of Saudi Arabia. The available evidence indicates that chronic inflammatory signaling involving CCL2, CCL5, TLR3, PTGS2/COX-2, IL-6/JAK/STAT3, NF-kB, and NLRP3 acts upstream of endothelial dysfunction, nitric-oxide/cGMP/PKG impairment, mitochondrial reactive oxygen species generation, and fibroblast activation. Extracellular-matrix regulators including ASPN, COL1A1, and MMP2 then amplify collagen deposition and myocardial stiffness, whereas mitochondrial genes and proteins such as ATP5C1 contribute to impaired oxidative phosphorylation, reduced ATP reserve, defective fatty-acid oxidation, and blunted mitophagy. Protein-quality-control pathways involving HSP90AA1, CCT2/CCT5, PSMA3, and stress-responsive STAT3 further link metabolic stress to proteotoxic injury. Epigenetic mechanisms, including DNA methylation and microRNAs such as miR-155, miR-1297, and miR-4649-3p, add a regulatory layer that may improve risk stratification but remains insufficiently validated for routine clinical use. In high-consanguinity settings, recessive cardiomyopathy variants can cluster in families and contribute to earlier NIHF presentations; however, population-level HFpEF-specific variant frequencies remain limited, and findings from HFrEF or dilated cardiomyopathy should be interpreted as candidate pathway evidence rather than definitive HFpEF markers. Translationally, SGLT2 inhibitors, mineralocorticoid-receptor antagonism, biomarker panels, and structured genetic evaluation provide the most clinically actionable bridge from molecular mechanisms to precision HFpEF care. - Source: PubMed
Publication date: 2026/07/11
Abou Al-Saud Sara