Rat Histone deacetylase 10,HDAC10 ELISA KIT
- Known as:
- Rat Histone deacetylase 10,HDAC10 Enzyme-linked immunosorbent assay test KIT
- Catalog number:
- E0855Ra
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- Btlab
- Gene target:
- Rat Histone deacetylase 10 HDAC10 ELISA KIT
Related genes to: Rat Histone deacetylase 10,HDAC10 ELISA KIT
- 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
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- Chronic non-bacterial osteomyelitis (CNO) is a rare autoinflammatory bone disease primarily affecting children and adolescents. Reliable biomarkers for diagnosis, disease monitoring, and prediction of disease course are lacking. This study demonstrates that, when compared to healthy participants, the proportion of 'pro-inflammatory' CD14CD16 'classical' monocytes is elevated in patients with CNO, before and after the initiation of treatment. Differential DNA methylation (200 hyper-, 162 hypo-methylated) profiles in monocytes from CNO patients affect key genes involved in immune regulation, including RUNX3, HOXA9, HLA-DMB, HLAB, MAP3K6, RXRB, CD163L1, MAP2, CDK6, HLA-G, HDAC10, and HLA-DQA1 genes. Notably, DNA methylation changes persist and potentially progress over time after the initiation of treatment with naproxen. In conclusion, patients with CNO display higher proportions of 'classical' monocytes when compared to healthy participants in conjunction with dysregulated DNA methylation patterns. Molecular alterations remain despite symptom relief with naproxen, suggesting progressive inflammation-mediated changes. - Source: PubMed
Publication date: 2026/05/15
Carlsson EmilGodoy-Tena GerardMorbach HennerGirschick Hermann JDissanayake DilanCharras AmandineBallestar EstebanHedrich Christian M - To investigate the mechanisms of histone deacetylase (HDAC) 10 inhibitors (HDAC10Is) action in endometriosis and the target molecules of HDAC10Is. - Source: PubMed
Aso SakiKurogi ShusakuKubo ShuichiHijiya NaokiAoyagi YokoKai KentaroKobayashi EijiNasu Kaei - 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