Ask about this productRelated genes to: HDAC10 antibody
- Gene:
- HDAC10 NIH gene
- Name:
- histone deacetylase 10
- Previous symbol:
- -
- Synonyms:
- DKFZP761B039
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-30
- Date modifiied:
- 2016-10-05
Related products to: HDAC10 antibody
Related articles to: HDAC10 antibody
- Esophageal cancer (EC) remains a highly aggressive malignancy with limited therapeutic options and poor prognosis. To address the shortcomings of conventional therapies, we developed a biomimetic, reactive oxygen species (ROS)-responsive nanoprodrug for synergistic photothermal-chemotherapy of EC. Tannic acid and ellagic acid were chemically linked via boronate ester bonds to form a polyphenol-based nanoparticle (TPE). The epidermal growth factor receptor (EGFR)-targeting peptide GE11 was subsequently introduced onto red blood cell membranes (RBCM) to obtain GE11-RBCM, which was then used to cloak the TPE nanoparticles, yielding GE11-RBCM@TPE. The resulting nanoplatform exhibited excellent photothermal conversion capability under near-infrared irradiation and selectively released the therapeutic payload in response to elevated ROS levels within the tumor microenvironment. In vitro studies showed enhanced cellular uptake in EGFR-overexpressing EC cells and markedly increased cell death following combined photothermal and chemotherapeutic treatment. In vivo, GE11-RBCM@TPE significantly inhibited tumor growth with negligible systemic toxicity and prolonged blood circulation. Transcriptomic analysis further revealed up-regulation of pro-apoptotic (PER1, HK2, BMF, DAPK2) and autophagy-related genes (ATP6V0D2, HDAC10, BNIP3, DEPP1, ATG9B, NAT16), while SQSTM1 and IL6 were down-regulated, indicating simultaneous activation of apoptosis and autophagy. These findings suggest that GE11-RBCM@TPE represents a promising strategy for precise and effective treatment of esophageal cancer. - Source: PubMed
Publication date: 2026/02/27
Chen YangZhu LiXu WeiChen QiTeng FeiBao KaiwenZhang LuWang YuanWu WeiWang Zhiqiang - Few advances have been made in the treatment of T-cell acute lymphoblastic leukemia (T-ALL). Approaches targeting histone deacetylases (HDAC) have not been thoroughly investigated in T-ALL. However, the underlying molecular mechanism of HDAC inhibition remains to be fully elucidated. - Source: PubMed
Publication date: 2026/02/04
Gu ZhenyangLiu YuchenJiao YifanWang HaoWang LiliLe NingZhang XiaweiLiu QingyangXu YangLiu DaihongGao ChunjiDou Liping - Exposure to fine particulate matter (PM2.5) represents a leading environmental cause of pulmonary inflammation and diseases, yet the underlying cellular mechanisms remain incompletely understood. Here, we identify histone deacetylase 10 (HDAC10) in macrophages as a critical regulator of PM2.5-induced airway inflammation by governing autophagic flux. PM2.5 exposure upregulated HDAC10 expression specifically in lung macrophages both in vivo and in vitro. Myeloid-specific Hdac10 deletion markedly attenuated PM2.5-induced airway inflammation and inflammatory cytokine production by inhibiting macrophage autophagy. Mechanistically, HDAC10 interacted with Beclin1 and deacetylated it at lysine 5 (K5), a modification critical for autophagic flux and subsequent inflammatory responses. Pharmacological inhibition of HDAC10 with salvianolic acid B reduced Beclin1 deacetylation, suppressed macrophage autophagy, and ameliorated PM2.5-induced lung inflammation. Clinically, elevated HDAC10 expression and reduced Beclin1 acetylation were observed in lung tissues from chronic obstructive pulmonary disease (COPD) patients, where HDAC10 mRNA levels correlated positively with the heightened lung inflammation. Our findings reveal a previously unrecognized HDAC10-Beclin1 axis that links PM2.5 exposure to macrophage autophagy and pulmonary inflammation, providing potential therapeutic targets for PM2.5-related respiratory diseases. - Source: PubMed
Publication date: 2026/01/16
Huang JiewenQuan JingyunSu GuomeiLuo ShutongZhao ZhaoLai XianwenZhong YuZang NiankeXiang YuanyuanHuang RuinaLi ShihaiLuo ChaoleChen JunfenGao XiaoDuan JielinLi YuyanLai Tianwen - Histone deacetylases (HDACs) are enzymes that remove acyl groups from histones and other proteins. This process leads to condensation of DNA and subsequent downregulation in expression of specific genes altering the activity of essential cellular pathways and changing the cell's behaviour. As a result, HDACs have emerged as potential therapeutic targets to treat different forms of cancer. In this study we synthesized and investigated compounds built around a phorbazole scaffold to characterize their histone deacetylase inhibitor (HDACi) activity. Eighteen phorbazole analogues were tested against class I and II HDACs in cell lysate, seven showed moderate activity, of which, three had IC values below 50 μM. The five best candidates were evaluated more extensively against HDAC1-11 (except for HDAC10). The best candidate, compound 9, initially appeared to reduce the activity of HDAC9 and HDAC11 by more than 50 % at 10 μM concentration. The binding mode of compound 9 to HDACs was explored via computational docking, where two poses stood out. These were explored further by molecular dynamic simulation. We found that 9 likely binds HDAC9 with the pyrrole group buried in the active site and forming H-bonds with the backbone oxygen of one of the glycine residues lining the cavity. But neither of the poses explored offered convincing arguments to describe the mode of action of the phorbazole, especially when comparing 9 to other analogues tested in this study. Additional experiments found that 9 interfered with the cell lysate assays by inhibiting luciferase in a dose-dependent manner (IC < 1 μM) and by exhibiting autofluorescence when tested on purified HDAC proteins, thereby confounding the obtained results during both the pan-HDAC screening and the single point HDAC inhibition assay. To address this, we employed fluorophores with excitation and emission wavelengths outside of the emission range of 9 and found that the HDAC inhibition potential of 9 was weaker than first observed. Finally, Compound 9 was found to be very soluble in water (418 μM) and membrane permeable (>48 % flux). This study highlights the need for rigorous validation of results. In our case, two orthogonal testing methods were not sufficient to catch all the confounding factors involved in measurement of HDAC inhibition, and a third approach was required to identify the actual inhibition of 9 against HDAC9 and 11. - Source: PubMed
Publication date: 2025/11/19
Reierth Ida Amalie NystadGuttormsen YngveAndersen Jeanette HHansen Espen HAbdelhady Ahmed MossadLanger Manuel KHaug Bengt ErikBayer AnnettePetit Guillaume A - Mono-2-ethylhexyl phthalate (MEHP), a major metabolite of diethylhexyl phthalate, is increasingly recognized as an environmental contaminant with potential cardiovascular toxicity. However, the molecular mechanisms underlying MEHP-induced atherosclerosis (AS) remain poorly understood. This study aimed to investigate the toxicological targets and pathways through which MEHP contributes to AS development using network toxicology approaches. DEGs associated with AS were identified from the GSE100927 dataset. MEHP targets were predicted using multiple databases including SEA, SwissTargetPrediction, and TargetNet. Common toxicological targets were identified through intersection analysis. Functional enrichment analysis, GSVA, and ssGSEA were performed. Machine learning algorithms including LASSO regression, RF, and SVM were employed to identify key targets. A nomogram model was constructed for AS risk prediction, and molecular docking analysis was conducted to validate protein-ligand interactions. Analysis identified 13,905 DEGs in AS, with 172 potential MEHP targets yielding 92 common toxicological targets. Enrichment analysis revealed involvement in calcium signaling, PPAR signaling, inflammatory response, and immune pathways. Machine learning identified three key targets: PDPK1, HDAC10, and HRH1. The nomogram model based on HDAC10 and HRH1 demonstrated excellent predictive performance. ssGSEA analysis revealed significant associations between key targets and immune pathways. Molecular docking confirmed strong binding affinities, with HRH1-MEHP showing the highest affinity. MEHP may promote AS via coordinated effects on calcium handling, receptor-mediated and transcriptional signaling, oxidative stress, apoptosis, and immune activation. HRH1, HDAC10, and PDPK1 emerge as mechanistic mediators and potential biomarkers, with an HDAC10/HRH1 nomogram offering translational utility for AS risk stratification; docking results provide testable hypotheses for mechanistic validation. - Source: PubMed
Publication date: 2025/11/17
Sun QiuZhao Gang