Rat Histone deacetylase 1,HDAC1 ELISA KIT
- Known as:
- Rat Histone deacetylase 1,HDAC1 Enzyme-linked immunosorbent assay test KIT
- Catalog number:
- E0854Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Rat Histone deacetylase 1 HDAC1 ELISA KIT
Related genes to: Rat Histone deacetylase 1,HDAC1 ELISA KIT
- Gene:
- HDAC1 NIH gene
- Name:
- histone deacetylase 1
- Previous symbol:
- RPD3L1
- Synonyms:
- HD1, GON-10, KDAC1
- Chromosome:
- 1p35.2-p35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2019-02-19
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- Histone deacetylases (HDACs) regulate neuroprotection; however, Trichostatin A (TSA), an HDAC inhibitor, lacks clear molecular mechanisms and core targets in Alzheimer's disease (AD), limiting clinical translation. This study aimed to decipher TSA's AD-regulating network, screen core genes, and support AD early diagnosis and multi-target therapies. - Source: PubMed
Publication date: 2026/04/20
Ou ChangzeChen BinbinDeng JunLong Huajun - Senile osteoporosis (SOP) is an age-related skeletal disorder characterized by progressive bone mineral density loss and deteriorated bone microarchitecture, imposing significant burdens on aging populations. Impaired osteogenesis of mesenchymal stem cells (MSCs) is a critical feature of SOP, yet its intrinsic mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/04/17
Pang PeizhuoChen JunhuaLi QiboSu ZepengLin JiajieZeng YipengZhang WeihaoXiao ZipengChen ZibinLiu ZiqianLin YangfengZheng GuanYu WenhuiXie Zhongyu - Epigenetic dysregulation plays a critical role in tumorigenesis and cancer progression. The development of isoform-selective histone deacetylase (HDAC) inhibitors has emerged as a promising strategy in cancer therapy. In this study, based on our previously identified hit compounds, a series of novel N-arylamide-quinoline derivatives were rationally designed and synthesized as HDAC isoform-selective inhibitors with improved efficacy and reduced toxicity. Among them, 6b exhibited potent inhibitory activity against HDAC1, 2, 3, and 10, while showing no activity against HDAC4-9, a selectivity profile further supported by molecular docking and molecular dynamics simulation. 6b demonstrated significant antiproliferative effects against HL-60, CCRF-CEM, and HepG2 cancer cells. In vitro toxicity assays revealed a high selectivity index for this compound, markedly superior to that of the parent compounds. Mechanistic studies showed that it induced hyperacetylation of histone H3 in a concentration-dependent manner, downregulated Rb protein and caspase-8 precursor, and modulated the expression of BAX, BAK, and BCL-2, leading to extrinsic apoptosis and G/G phase cell cycle arrest. In vivo, 6b exhibited potent antitumor activity with no apparent toxicity following both intragastric administration and intraperitoneal injection. Notably, intraperitoneal delivery resulted in enhanced efficacy. Pharmacokinetic studies further characterized the in vivo behavior of this compound via both routes. Overall, hit compound 6b displays favorable biological properties and represents a promising candidate for further anticancer drug development, with subsequent studies focusing on the optimization of its drug-like properties. - Source: PubMed
Publication date: 2026/04/13
Yu BingyanWang NingLou GaojieWu LingjieWang YuleYin SijiaLu YiXu JunWang ZeChen XinyuanHe ShanZhang Bin - How CoREST-linked chromatin activities are regulated at promoters independently of canonical REST repression remains unclear. Here, we identify the zinc-finger proteins rearranged L-myc fusion (RLF) and ZFP292 as redundant promoter-associated factors that stabilize CoREST-linked LSD1 engagement within RCOR2-containing CoREST assemblies at active and bivalent promoters in embryonic stem cells. Loss of RLF/ZFP292 reduces ZMYM3 occupancy while diminishing LSD1 enrichment at target promoters, whereas RCOR2 and HDAC1 occupancy remain largely unchanged, consistent with a role in stabilizing enzymatic engagement rather than in complex recruitment. Loss of RLF/ZFP292 increases promoter-associated active chromatin features at both promoter classes, but transcriptional upregulation is most evident at genes with bivalent promoters. At a subset of active promoters, selective loss of ZMYM3 coincides with reduced transcription despite retained RCOR2-HDAC1-LSD1 signals. Together, these findings reveal a REST-independent mechanism in which RLF/ZFP292 modulate the functional output of promoter-associated CoREST assemblies to maintain transcriptional balance in pluripotent cells. - Source: PubMed
Publication date: 2026/04/16
Ito TakamasaYoshino MasahitoIsobe Shin-YaObuse Chikashi - Diabetic kidney disease (DKD) is characterized by renal lipid accumulation, but the molecular mechanisms underlying this lipotoxic phenotype remain unclear. Secreted frizzled-related protein 2 (SFRP2) has been implicated in metabolic regulation, yet its role in renal cholesterol homeostasis and DKD pathogenesis is unknown. - Source: PubMed
Publication date: 2026/04/15
Lv DanLin ZiyueYang JiakunLi WuchaoWu KeqianPeng RuiLiu HandengZha HeRuan Xiong ZhongLiao XiaohuiSun YanZhang Zheng