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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- During long-term artificial selection, China has developed indigenous dairy goat populations with breed-specific traits and environmental adaptability. However, the genetic relationships and genomic characteristics of these populations remain insufficiently studied. - Source: PubMed
Publication date: 2026/08/06
Xiong JinkeShang MingyuBao JingjingLiu TianyiYang PeifuSun XintianJiang YutingZhang Li - The evasion of programmed cell death significantly contributes to therapeutic failure in cancer, with resistance to apoptosis being the most prevalent form of resistance in multidrug-refractory diseases. Ferroptosis, an iron-dependent, non-apoptotic form of regulated cell death characterized by the lethal accumulation of lipid peroxides, represents a pharmacologically significant vulnerability in cancers that are resistant to apoptosis and tolerant to drugs. The resistance to ferroptosis, induced by the aberrant overexpression of the epigenetic enzyme histone deacetylases (HDACs) and the sustained transcriptional activity of key antiferroptotic targets, particularly GPX4 and SLC7A11, is enforced through epigenetic mechanisms. This review examines the extant preclinical and translational data, demonstrating that HDAC inhibitors predispose cancer cells to ferroptosis through four mechanistically convergent pathways. These pathways include the transcriptional silencing of SLC7A11 and subsequent glutathione depletion, disruption of intracellular iron homeostasis via ferroportin downregulation, enhancement of mitochondrial ROS-induced lipid peroxidation, and suppression of the HDAC3-NRF2-GPX4 antiferroptotic axis. The specific roles of HDAC1, HDAC3, and HDAC10 in colorectal, lung, gastric, and hematological cancers are elucidated. Additionally, the review discusses hybrid molecules of HDAC-ferroptosis, combination strategies with GPX4 inhibitors, and immunochemotherapy. Considerations such as isoform selectivity, biomarker development, and clinical translation are addressed, highlighting HDAC inhibitor-mediated ferroptosis sensitization as a promising strategy to overcome drug resistance in cancer. See also the graphical abstract(Fig. 1). - Source: PubMed
Publication date: 2026/07/08
Alamri Mubarak AAfzal MuhammadPandey Surya NathAfzal ObaidAkela Mohamed AhmedRekha A - Nasopharyngeal carcinoma (NPC) is an aggressive head and neck malignancy in which post-treatment recurrence and distant metastasis remain major contributors to poor clinical outcomes. Although microRNAs are important post-transcriptional regulators of tumor progression, the role of miR-320d in NPC remains incompletely understood. This study evaluated the biological role of miR-320d and explored whether it is involved in regulating neutrophil extracellular trap (NET) formation through the nuclear factor kappa-B (NF-κB)/interleukin-8 (IL-8) signaling axis. miR-320d was overexpressed in NPC cell lines S18 and 5-8F, and cell viability, migration, and invasion were evaluated. Integrated transcriptomic and proteomic analyses were performed to identify miR-320d-regulated genes, proteins, and pathways. Western blotting, immunohistochemistry, and immunofluorescence analyses were used to validate NET-associated proteins, including glycoprotein Ib platelet subunit alpha (GP1BA), histone deacetylase 10 (HDAC10), and fibrinogen gamma chain (FGG), as well as the expression of NET formation markers, including peptidyl arginine deiminase 4 (PADI4), myeloperoxidase (MPO), and neutrophil elastase (NE); and key components of the NF-κB/IL-8 axis. miR-320d overexpression significantly inhibited the viability, migration, and invasion of both S18 and 5-8F cells. Multi-omics analyses indicated that miR-320d-regulated molecules were mainly enriched in NET-related pathways. Consistently, miR-320d reduced the expression of GP1BA, HDAC10, FGG, PADI4, MPO, and NE. Mechanistically, miR-320d suppressed NF-κB signaling, as shown by decreased phosphorylated NF-κB (p-NF-κB) and total NF-κB levels, and reduced IL-8 secretion in NPC cells. miR-320d may suppress NPC progression, at least in part, by attenuating NF-κB/IL-8-associated NET formation. These findings suggest that the miR-320d/NF-κB/IL-8/NET regulatory axis may participate in NPC progression and may warrant further translational investigation. - Source: PubMed
Publication date: 2026/07/16
Liu LiuLiu JieNing ShuangchenWang JinHe Yingchun - Although immune checkpoint blockade has offered new hope to patients with bladder cancer, its overall response rate remains modest. In this setting, the quantity and functional status of CD8+T cells largely dictate therapeutic efficacy. Integrative bioinformatics analyses, validated in our institutional tissue cohort, we demonstrated that histone deacetylase 10 (HDAC10) was markedly up-regulated in bladder cancer and inversely correlated with CD8+T cells infiltration. In vivo experiments, using Hdac10-KO cell line, we revealed that Hdac10-KO significantly inhibited tumour growth and promoted the infiltration and activity of CD8+T cells. Mechanically, HDAC10 deacetylated the K342 site of interleukin enhancer-binding factor 3 (ILF3), thereby inducing the ubiquitination and degradation of it by WWP2. This reduced the stability regulation of CXCL9 mRNA by ILF3, decreasing CXCL9 expression and weakening CD8+T cell infiltration and activation. Notably, we found that the probiotic Clostridium butyricum (C.B.) can inhibit the expression of HDAC10 by increasing the short-chain fatty acid butyric acid, thereby sensitizing immunotherapy for bladder cancer in mouse models. This study revealed the specific mechanism by which HDAC10 led to immunotherapy resistance in bladder cancer and proposed potential combined treatment strategies. - Source: PubMed
Publication date: 2026/07/13
Zhuang JuntaoYu HaoChen YuhanSun HuanyouShen AoJiang LinjingBai RongjieTan ZhengyeLv JianchengBai KexinWang WeiYang HaiweiYang XiaoLu Qiang - Triple-negative breast cancer (TNBC) remains a clinical challenge due to the lack of druggable targets, an immunosuppressive tumor microenvironment (TIME), and the limited efficacy of immune checkpoint inhibitors (ICIs). Herein, we report the first rational design, synthesis, and evaluation of dual PAK1/HDAC10 inhibitors to concurrently suppress oncogenic signaling and influence the TIME. Optimization yielded , which displays nanomolar potency against PAK1 and HDAC10, excellent selectivity for HDAC10, and negligible off-target kinase activity. Mechanistically, coinhibits PAK1 oncogenic signaling and HDAC10 epigenetic regulation, downregulates PD-L1, and modulates the TME by reducing MDSC/Treg infiltration while enhancing CD8 T-cell infiltration and activation. , exhibits favorable pharmacokinetics, robustly suppresses tumor growth and pulmonary metastasis in TNBC models, and demonstrates a clean safety profile. These findings demonstrate that dual targeting of PAK1 and HDAC10 is a promising therapeutic strategy for TNBC, and represents a valuable preclinical candidate for further development as an immunomodulatory antitumor agent. - Source: PubMed
Publication date: 2026/07/08
Chen WeijiCheng XiaolingZhao XiChen ZixuanLai YupeiHao WenliHe ZhendanLin WenhongWu YanGuo YapingPan DaboZhou LeYao Dahong