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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- Inflammation and infection are responsible for the majority of early preterm births. Host innate immune responses at the maternal-fetal interface that contribute to sterile intra-amniotic inflammation (SIAI), bacterial clearance, or invasive infection remain poorly understood. Group B Streptococcus ( ) is a leading cause of preterm birth, stillbirth, and invasive neonatal disease. - Source: PubMed
Publication date: 2026/09/17
Manuel GygeriaColer CelesteMunson JeffCornelius JohnDuell TylaKim TaeyunVo AndrewOrvis AustynColeman MichelleMurphy KyleeZhao HongSun SidneyChima Sophia CSindhu VanshikaHuang HazelLi AmandaLi MirandaEnglish ChrisBaldessari AudreyDel Rosario BrianaCervantes OrlandoKapur RajRajagopal LakshmiAdams Waldorf Kristina M - Tumor maturation is a property of neuroblastomas but can also be observed in unique cases of primary brain malignancies. We hypothesized that the mechanisms of peripheral and central neurogenic tumor maturation could be similar. This study encompassed 19 cases of neuroblastoma and solitary cases of CNS tumors having undergone a morphologically verified maturation. The tumors were analyzed by sequencing and gene expression profiling. We revealed potential similarity of different tumor types upon maturation, associated with stimulated MAPK, PI3K-AKT-mTOR, and TrkA signaling and suppressed regulation of cell cycle and DNA replication and repair. Tumors completing maturation similarly showed enhanced immunogenicity. The levels of NTRK2 expression increased during maturation. Expression of NTRK1 and positive epigenetic regulators (SWI/SNF subunits) increased prior to maturation and decreased upon the differentiation completion. Expression of negative epigenetic regulators EZH2, HDAC10, HDAC2, and DNMT3A decreased in maturing tumors. These data suggest that central and peripheral neurogenic tumors are likely to have common maturation mechanisms. Molecular scenarios associated with neuroblastoma maturation could be: (1) TrkA signaling (seen in cases presenting in < 18-month-olds), or (2) altered expression of epigenetic regulators and transcription factors (seen in cases presenting in >18-month-olds); treatment-induced maturation of CNS malignancies could involve both scenarios. - Source: PubMed
Publication date: 2026/09/11
Druy Alexander EZverev Ivan AAndreeva Natalia ATarakanova Alexandra VSenchenko Maria AGegeliya Nina VZaytseva Margarita ASanakoeva Agunda VPanferova Agnesa VAbasov Ruslan KUsman Natalia YPetrova Vera SKonovalov Dmitry MRaskin Grigorii ANovichkova Galina AGrachev Nikolay SShamanskaya Tatyana VKachanov Denis YPapusha Ludmila I - 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