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) are potent regulators of gene expression, yet incomplete understanding of individual HDAC function coupled with the lack of selective inhibitors has impeded successful targeting of these proteins for the improvement of human health. Although all HDAC proteins contain a deacetylase domain, the 18 distinct human HDAC proteins have remarkably distinct mechanisms of action. In a misleading oversimplification, HDACs are often thought to uniformly deacetylate histones to affect global gene expression in a functionally redundant manner. Instead, findings continue to define the distinct roles of individual HDACs, highlighting the potential value of data-driven precision targeting of individual HDACs or specific subclasses of HDACs for disease therapy. Here, we will discuss this decade's advances about how the zinc-dependent HDACs, HDAC1 to HDAC11, regulate gene expression in health and disease. - Source: PubMed
Publication date: 2026/06/05
Van Bree Bryce AEichner Lillian J - Chemoresistance severely limits therapeutic options for advanced bladder cancer. Histone deacetylases (HDACs) have been implicated in tumour progression and treatment resistance, yet their role in acquired chemoresistance remains incompletely defined. We investigated whether epigenetic modulation could restore chemotherapy sensitivity in drug-refractory bladder cancer. - Source: PubMed
Publication date: 2026/05/11
He YiruiFang ZaixiangZhang JiapengWei QiangLi YunkunDuan ZhenyuXu GangLin TianhaiXiong QiaoGong QiyongTan PinLuo Kui - HDAC6 is a promising therapeutic target for the treatment of cancer and neurodegenerative and inflammatory diseases. We have developed a thiazolyl alkyl hydroxamate scaffold as an HDAC6-selective inhibitor. Herein, we synthesized new thiazolyl hydroxamate derivatives to investigate the effects of aliphatic linker length and cap group rigidity on HDAC6 selectivity. Hydroxy-3-(2-(6-methoxynaphthalen-2-yl)thiazol-4-yl)propanamide () was identified as a potent HDAC6 inhibitor (IC = 25.56 nM) with ∼500-fold selectivity over HDAC1. Docking and MD simulations revealed that the 6-methoxy-β-naphthalene cap of stably occupies a hydrophobic pocket containing HDAC6-specific nonconserved residues, providing a rationale for novel HDAC6 inhibitor design. Treatment with upregulated BDNF (exons I and IV), and other neurogenesis-related genes in neural progenitor cells. In vivo, improved memory performance in scopolamine-treated memory-impaired mice in the passive avoidance test. These findings suggest that enhances neuroplasticity-related pathways and warrants further investigation as a potential therapeutic candidate for neurodegenerative diseases. - Source: PubMed
Publication date: 2026/06/04
Nam GibeomJung Jun MinYang SeyunKim Da EunBoggu Pulla ReddyKim CheolheeKim EunaeJo ChanheeYang Hyun-MoKim JihunJang Choon-GonChung Sang JSul Jae HoonJo Dong-GyuJung Young HoonPark Hyun-Ju - The precise balance between human trophoblast stem cells (hTSCs) self-renewal and differentiation into syncytiotrophoblasts (STBs) is essential for proper placental development. While the transcriptional and signaling networks regulating this process have been extensively studied, the contribution of protein homeostasis remains poorly understood. Here, we identify FBXO22, the substrate recognition subunit of the SCF E3 ubiquitin ligase complex, as a key regulator of trophoblast fate. We found that FBXO22 was enriched in the nuclei of cytotrophoblasts (CTBs) and levels were reduced markedly in early placental villi from patients with recurrent pregnancy loss (RPL). Experimental loss of FBXO22 compromised hTSC stemness and led to aberrant premature differentiation toward STBs. Mechanistically, FBXO22 selectively ubiquitinates and destabilizes the CoREST complex, thereby coordinating with HDAC1 and LSD1 to regulate histone modifications, including H3K27 acetylation (H3K27ac) and H3K9 dimethylation (H3K9me2). Disruption of this nuclear ubiquitination pathway perturbs the balance between proliferation and differentiation, ultimately impairing placental development. Our findings uncover a previously unrecognized nuclear role of FBXO22 in maintaining cellular homeostasis, linking ubiquitin-mediated protein degradation to trophoblast fate determination and providing new insights into the molecular pathology underlying early pregnancy loss. - Source: PubMed
Li HongliSong GuangminZhou LinweiZhang ManLi YunLiu XinmiWang XingYang LiTao XinyiCannon Richard DSaffery RichardNovakovic BorisQi HongboZhou XiaoboZhang Hua - The DNA damage response (DDR) is critical for pancreatic ductal adenocarcinoma (PDAC) development and therapeutic responses, including to genotoxic agents. While epigenetic modulators have been shown to contribute to the DDR, how chromatin regulation dictates responses to DNA damage in PDAC remains incompletely understood. Here, we identify Class I histone deacetylases (HDACs) as critical regulators of the DDR. HDAC1/2 directs the genomic distribution of H3K27ac, ensuring sufficient BRD4 and RNA polymerase II (Pol II) occupancy at DDR gene promoters. HDAC inhibition by entinostat shifts the balance of H3K27 acetylation preferentially towards intergenic regions, diverting BRD4 and Pol II from promoters, thereby suppressing DDR gene expression. In line with this, HDAC inhibition heightens DNA damage and sensitizes PDAC to diverse DNA-damaging and DDR-targeting agents. Since the clinical development of HDAC inhibitors has been limited by systemic toxicity, we developed bottlebrush prodrug (BPD) nanoparticles for tumor-selective entinostat delivery. Entinostat-BPD achieved tumor-specific HDAC inhibition while displaying potent efficacy and reduced systemic toxicity. These findings reveal an HDAC-dependent DDR vulnerability and offer combinational and precision targeting strategies to facilitate clinical translation and improve PDAC patient outcomes. - Source: PubMed
Publication date: 2026/05/19
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