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
- Heat stress negatively affects bovine fertility and embryonic development, while cryopreservation imposes additional cellular stress that may impair embryo survival. The present study investigated whether controlled heat treatment applied during the early morula stage could influence subsequent blastocyst development, molecular stress responses, and post-thaw survival of bovine embryos. In vitro-produced bovine embryos were exposed to controlled thermal treatment involving gradual elevation in temperature from 38.8 °C to 40.0 °C followed by subsequent cooling. Blastocyst formation, post-thaw survival after slow freezing, and the expression of stress-associated genes and microRNAs were evaluated. Heat treatment did not significantly affect blastocyst formation rates or post-thaw embryo survival compared to the control groups. However, significant alterations in the expression of stress-associated markers were observed. The expression of HSP90AA1 and HSPB11 was significantly reduced following heat treatment, while cryopreservation induced increased expression of these markers compared to embryos exposed only to heat treatment. Significant alterations were also detected in the expression of several stress-associated microRNAs. These findings suggest that controlled heat exposure during the morula stage may induce molecular changes associated with the embryonic response to heat stress without compromising developmental competence or cryosurvival. The results contribute to a better understanding of the molecular mechanisms underlying embryonic responses to thermal and cryogenic stress and may support future optimization of embryo production and cryopreservation strategies. - Source: PubMed
Publication date: 2026/07/23
Nagy KatalinSzabadi Nikolett TokodynéGócza ElenLázár BenceEcker AndrásTóth ArnoldSándorová LillaStéger ViktorTokár AlexandraGustavo DelgadoZomborszky ZoltánBodó Szilárd - Dibutyl phthalate (DBP) is a ubiquitous environmental plasticizer that has been associated with metabolic dysfunction and steatotic liver injury. Hesperetin, a citrus flavonoid, has reported hepatoprotective properties, but its potential protective mechanisms against DBP-associated steatotic liver injury remain incompletely characterized. - Source: PubMed
Publication date: 2026/08/06
Zhou ShiwenLi ShaZhao YueShi HuZhao Yueliang - is a classic medicinal and edible plant with great exploitation potential in anti-inflammatory research. This study aimed to explore its anti-ulcerative colitis bioactive constituents and corresponding mechanisms of action. A total of 15 flavonoids and coumarins were identified by macroporous resin purification combined with ultra-performance liquid chromatography coupled to UPLC-Q-Exactive Orbitrap MS/MS. Seven key bioactive compounds (eupatilin, cirsimaritin, quercetin, scoparone, 7-hydroxycoumarin, scopoletin and esculetin) and six core targets (TNF, AKT1, SRC, EGFR, HSP90AA1 and ESR1) were further screened via network pharmacology. Subsequent molecular docking analysis verified that flavonoids exhibited markedly stronger binding affinity to target proteins than coumarins. In vitro cellular experiments revealed that eupatilin exhibited the strongest anti-inflammatory activity among all key components. In vivo animal assays further validated that eupatilin alleviated colonic injury and markedly reduced the levels of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 in mice with DSS-induced ulcerative colitis. This work provides vital experimental evidence for the development and utilization of anti-ulcerative colitis ingredients from , and validates its promising health-related application value in the food industry. - Source: PubMed
Publication date: 2026/07/27
Zhang PanpanXu XinyuChen YongjieSuo YizhenZhang Yuhong - Breast cancer remains a major cause of morbidity and mortality in women, with around 2.3 million new cases and 670,000 deaths worldwide in 2022. Daidzin, a soy isoflavone glycoside from Glycine max, is a candidate bioactive scaffold, but its breast cancer-relevant mechanisms remain poorly defined. This study used an integrated in silico strategy combining network pharmacology and molecular modeling to prioritize daidzin targets and validate key interactions, with sirtinol as a reference compound. Target prediction identified 101 putative daidzin targets, and intersection with breast cancer-associated genes yielded 97 common targets. Protein-protein interaction analysis highlighted hub genes including ALB, TNF, MMP9, CASP3, SRC, ITGB1, MMP2, ESR1, IL2, and HSP90AA1. Enrichment analyses suggested convergence on extracellular/vesicle-related functions, metallopeptidase activity, and pathway modules spanning metabolism, inflammation, endocrine signaling, and cancer circuitry. Docking against ten hub proteins produced binding energies from -6.00 to -11.49 kcal/mol, with the strongest affinity for MMP9 (6ESM; -11.49 kcal/mol), exceeding B9Z (-10.54 kcal/mol) and sirtinol (-10.59 kcal/mol). Molecular dynamics simulations indicated stable complexes, and Molecular Mechanics Generalized Born Surface Area (MMGBSA) supported stronger binding for daidzin-MMP9 (-46.86 ± 3.83 kcal/mol) than sirtinol-MMP9 (-14.12 ± 8.99 kcal/mol). Absorption, Distribution, Metabolism, Excretion, and Toxicity (ADMET) prediction indicated favorable safety-related flags for daidzin, although lower predicted intestinal absorption and Caco2 permeability than sirtinol suggest potential exposure-related limitations. Density Functional Theory (DFT) analysis supported comparatively greater electronic stability. Collectively, the results prioritize a daidzin-MMP9 axis for experimental validation. - Source: PubMed
Publication date: 2026/08/11
Vu Lan ThiVu Luong TrongVu Lien Thi KimPho Hang Thi ThuyNguyen Quan HuuNguyen Lan Thi NgocNguyen Yen Thi HaiNguyen Hung DucChu Mau Hoang - Acute kidney injury (AKI) is a severe clinical syndrome, with ischemia/reperfusion (I/R) being one of its most common causes. Although D‑pinitol (DP), an inositol‑like bioactive molecule, is known to confer renal protection, its efficacy against I/R‑induced AKI remains unknown. A mouse kidney I/R model was employed to evaluate the renoprotective effect of DP. Relevant targets associated with DP and AKI were retrieved from publicly available databases. Subsequently, network pharmacology analysis was conducted to identify the potential targets and signaling pathways. Molecular docking was then performed to predict the binding affinity of DP to core targets identified. Furthermore, and experiments were performed to validate these findings. Systemic toxicity was assessed by serological and histopathological examinations. The results show that DP significantly attenuated I/Rinduced kidney dysfunction and apoptosis. Network pharmacology analysis identified 108 overlapping targets, with AKT1, HSP90AA1, SRC, CASP3, and MMP9 identified as core targets. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed PI3K/AKT signaling pathway as the primary mechanism. Consistent with these predictions, DP enhanced PI3K and AKT phosphorylation in kidney tissue. Molecular docking indicated that DP exhibited the strongest binding affinity to SRC, suggesting it as a potential target. In a hypoxia/reoxygenation (H/R)-induced human renal proximal tubular epithelial (HK-2) cell model, DP significantly increased the phosphorylation of SRC, PI3K, and AKT, and these effects were abrogated by the SRC specific inhibitor PP2. Collectively, DP alleviated I/R‑induced injury and apoptosis, potentially through activation of the SRC/PI3K/AKT signaling pathway. - Source: PubMed
Publication date: 2026/08/10
Ren YilinGe YuanZhang KeyuLin HuiNiu DanHan WeixiaSu XiaoleWang LihuaQiao Xi