Ask about this productRelated genes to: HSP90AB1 Blocking Peptide
- Gene:
- HSP90AB1 NIH gene
- Name:
- heat shock protein 90 alpha family class B member 1
- Previous symbol:
- HSPC2, HSPCB
- Synonyms:
- -
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-27
- Date modifiied:
- 2016-10-05
Related products to: HSP90AB1 Blocking Peptide
Related articles to: HSP90AB1 Blocking Peptide
- Primary dysmenorrhea (PD), a prevalent gynecological disorder, is fundamentally driven by chronic uterine inflammation, leading to severe lower abdominal pain and recurrent cramping. Given the known anti-inflammatory properties of Puerarin (Pue) and Dehydroepiandrosterone (DHEA), we investigated their individual and combined therapeutic effects on PD using an estradiol benzoate/oxytocin-induced mouse model. Our findings revealed that both Pue and DHEA alleviated PD symptoms, as evidenced by reduced writhing frequency, prolonged inter-writhe intervals, diminished uterine edema, lower uterine PGF2α/PGE2 ratio, decreased levels of inflammatory cytokines, and downregulated endometrial cyclooxygenase-2 (COX-2) expression. Notably, co-administration of Pue and DHEA produced superior therapeutic efficacy. Mechanistically, this combination more effectively reversed the pathological upregulation of Hsp90ab1 and the heightened phosphorylation of p38 and JNK in the PD uterus. However, lentiviral overexpression of Hsp90ab1 significantly attenuated the therapeutic benefits conferred by Pue and DHEA. Collectively, these results demonstrated that the synergistic action of Pue and DHEA represents a potent therapeutic strategy for PD, primarily through suppression of the Hsp90ab1/p38/JNK signaling and subsequent mitigation of uterine inflammation, offering a promising avenue for clinical intervention. - Source: PubMed
Publication date: 2026/04/23
Zhu ZhengquanRuan JianguoWang RuizheWang YihanChen HaiyunYu XinyeWen YantingWang YongWang DaojuanTao Gaojian - Maxim (DrT) is a well-known traditional medicinal and edible plant with hepatoprotective effects. In this study, crude polysaccharides of DrT (DrTPs) were obtained using the water extraction-ethanol precipitation method. Autoimmune hepatitis (AIH) models of both mice and ALM12 cells were produced by ConA. The serum liver function indexes (AST and ALT) were examined by ELISA, and liver tissue pathological changes were observed by HE staining. The hepatoprotective mechanism of DrTP80 was explored by RNA sequencing and verified by detecting the protein expressions using Western blot. As a result, DrTP80 could significantly reduce AST and ALT levels in the injured liver and ALM12 cells. DrTP80 also obviously improved the hepatopathological changes in liver tissue induced by ConA. Furthermore, RNA sequencing detected significant differences in gene expression, and the functions of differential genes were focused on TNF and IL-17 signaling pathways. Based on these two signaling pathways, 13 differentially expressed genes (Vcam1, Atf6b, Akt1, Irf1, Map2k3, Lcn2, Hsp90ab1, Anapc5, Traf4, Fosl1, Jun, Cxcl5, Nfκbia) among NC, CRC, and FP groups were screened and verified by Western blot. In conclusion, our results demonstrated that DrTP80 can alleviate immune liver damage induced by ConA, and its hepatoprotective mechanism may be related to regulating TNF and IL-17 signaling pathways. Our findings indicated that DrTP80 could be exploited as a healthy food supplement for the treatment of immune liver injury. - Source: PubMed
Publication date: 2026/03/24
Guo MinWei SaixueCheng BiaobiaoLi Xiaodong - We examine how antibiotic misuse may induce gut dysbiosis, which influences the neurotoxicity of co-exposure to the environmental neurotoxicants Aflatoxin B (AFB) and Diethylnitrosamine (DEN) in rats. Wistar rats (n = 45; male) were assigned to Control, DEN (200 mg/kg, i.p.), or AFB (2 mg/kg, i.p.) groups, each further divided into saline, Ampicillin (50 mg/kg; p.o), or Ciprofloxacin (12.5 mg/kg; p.o) treatments over 21 days-14 days of antibiotics followed by 7 days of AFB or DEN co-treatment. Rat behaviour was assessed through the open field test, sucrose splash test, and Morris's water maze. Biochemical analyses measured neurotransmitters, oxido-nitrosative stress (ONS), inflammation, and apoptosis markers in the prefrontal cortex and hippocampus. The mechanisms and pharmacokinetics of the compounds were investigated using network pharmacology, molecular docking, and ADMET analyses. Antibiotic co-treatment reduced locomotion and exploration, increased anxiety, and impaired memory and learning across all tests. The co-treated groups demonstrated increased AChE activity, decreased antioxidant biomarkers, and heightened ONS and apoptosis in the prefrontal cortex and hippocampus. Network pharmacology identified 31 common targets among antibiotics, AFB/DEN, and oxidative-stress-related neurotoxicity. STAT3, HSP90AB1, EGFR, MMP2, KDR, and PDGFRB emerged as core hub genes. PPI and enrichment analyses highlighted their roles in kinase signalling, cell death regulation, and cancer pathways. Molecular docking indicated strong binding of AFB and CPX to HSP90AB1 and EGFR, suggesting potential interference with oxidative and apoptotic pathways. ADMET assessment showed antibiotics possess favourable drug-like properties, whereas AFB1 and DEN are more toxic, lipophilic, and neurotoxic, supporting their role in cortico-hippocampal injury. Antibiotic misuse may intensify the neurotoxic effects of AFB and DEN by increasing oxido-inflammatory responses and neuronal damage, leading to memory impairment and heightened anxiety-like behaviours. Addressing antibiotic misuse and promoting gut microbiota could improve brain health. - Source: PubMed
Publication date: 2026/04/15
Owumi SolomonOlabisi Taye PreciousChimezie JosephEso Victor OOwolabi Oluwaseun MSanusi Abdullah ABabalola Jesutosin OAkomolafe Ayomide PArunsi Uche OIrozure Chioma E - Acute respiratory distress syndrome (ARDS) is a life-threatening complication of sepsis, characterized by refractory hypoxemia and pulmonary inflammation. Currently, effective pharmacological interventions remain limited. Traditional Chinese medicine (TCM), exemplified by Dachengqi Decoction (DCQD), has demonstrated therapeutic potential in modulating complex inflammatory responses. To investigate the mechanism of DCQD in ARDS treatment, active components of DCQD and their associated targets were first retrieved from public databases. ARDS-related targets were identified through bioinformatics analysis of public datasets. By intersecting drug-specific targets with disease-related targets, a DCQD-ARDS interaction network was constructed using protein-protein interaction (PPI) analysis and functional enrichment. Comprehensive analysis revealed 32 overlapping genes critical to DCQD's therapeutic efficacy in ARDS. Enrichment analysis highlighted key pathways, including the chemokine signaling pathway, NOD-like receptor signaling, and neutrophil extracellular trap (NET) formation, which are implicated in immunomodulation and inflammation. The PPI network identified HSP90AB1, MMP9, HSP90AA1, ARG1, and MYC as core targets. Molecular docking confirmed strong binding affinities between these targets and DCQD components. Our findings untangle the mechanistic basis supporting DCQD as a promising adjunctive therapy for sepsis-induced ARDS. - Source: PubMed
Publication date: 2026/03/27
Gu DaGuo Qiang - Recent advances in targeted covalent inhibition have broadened the therapeutic landscape via the development of warheads that target various nucleophilic amino acids. Although cysteine was once the primary focus of such efforts, lysine has emerged as another appealing residue for covalent modification, due to its high prevalence within the proteome, functional importance, and low mutation rate. Despite this amino acid's reduced nucleophilicity at physiological pH, rational, structure-based techniques have enabled the identification of inhibitors that exploit the unique protein microenvironment that a given lysine occupies. Strategies to inhibit Hsp90 via covalent modification of Lys58 include the use of N-acyl-N-aryl sulfonamide (ArNASA) warheads and sulfur(VI) fluoride exchange (SuFEx) chemistry, both of which have demonstrated enhanced cellular selectivity and potency. However, such compounds fail to distinguish between the > 95% identical nature of the ligand binding sites in cytosolic Hsp90α and Hsp90β. In this study, the incorporation of electrophilic warheads onto Hsp90β-selective inhibitors resulted in compounds that demonstrate favorable binding to Hsp90β, yet subsequent analyses to confirm covalent modification of Lys58 were inconclusive. Nevertheless, the kinetics of inhibitor binding to the Hsp90 N-terminal ATP-binding pocket were obtained, whereby some compounds exhibited their highest affinity towards Hsp90β after a 2 h incubation. - Source: PubMed
D'Amico TerinReynolds Tyelor SSerwetnyk Michael ABlagg Brian S J