Ask about this productRelated genes to: HDAC1 antibody
- 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
Related products to: HDAC1 antibody
Related articles to: HDAC1 antibody
- To investigate whether MLKL crotonylation is associated with tubular autophagy-lysosome pathway homeostasis in lupus nephritis (LN) and to explore its relationship with RAB1A-mechanistic target of rapamycin (mTOR) signalling. - Source: PubMed
Publication date: 2026/08/31
Lu Rui-LingMeng Shu-HuiPeng Quan-ZhouChen YanranYang XufaLiu Hong YangZheng Feng-PingLiu DongzhouHong Xiaoping - Parkinson's disease (PD) is the second most common neurodegenerative disorder mainly characterized by the degeneration of dopaminergic neurons originating in the substantia nigra (SN) pars compacta and projecting to other brain regions, giving rise to motor and non-motor symptoms. Despite significant progress in understanding the molecular and cellular disruptions associated with PD, there remains an unmet clinical need for effective therapies. In this study, proteomic analysis of the olfactory tract (OT) in controls with no known neurological history (n = 17) and PD subjects (n = 21) revealed Lewy body disease (LBD) stage-dependent proteostatic impairment, accompanied by progressive modulation of the alpha-synuclein (α-syn) functional interactome. Differential OT omic profiles were used in a computational drug repurposing approach, revealing the HDAC1 inhibitor pyroxamide as one of the top drug candidates with in silico potential to restore altered OT omic profiles. To explore the potential therapeutic effects of pyroxamide, in vitro assays were performed using α-syn preformed fibrils (PFFs). Pyroxamide treatment reduced α-syn PFFs-induced toxicity in olfactory epithelial, microglial and dopaminergic neuronal cell lines, producing a protective effect against hydrogen peroxide-induced damage exclusively in brain-derived cell types. Mechanistically, the mitigating effects of pyroxamide were attributable, at least in part, to the regulation of Bax-1 and sirtuin 1 (SIRT1) protein expression, along with alterations in the mRNA levels of NEF2L2, IL1B, and TNF-α. These findings confirm the suitability of omics profiles in drug repurposing workflows against PD, offering valuable insights into the potential of HDAC1 inhibitors in the therapeutic pipeline of PD. - Source: PubMed
Publication date: 2026/08/30
Cartas-Cejudo PazDe Miguel MarinaExtramiana LeireLachén-Montes MercedesRomero-Murillo SilviaGveric DjordjeFernández-Irigoyen JoaquínSantamaría Enrique - Histone deacetylase 6 (HDAC6) is predominantly localized in the cytoplasm with nucleocytoplasmic shuttling capability. Featuring two tandem catalytic domains and a C-terminal ubiquitin-binding domain, it primarily deacetylates non-histone substrates such as α-tubulin and HSP90. This distinct subcellular localization and substrate profile endow HDAC6 with the unique capacity to orchestrate pivotal roles in cytoskeletal regulation, the cellular stress response, protein degradation, and cell migration, thereby positioning it as a highly attractive target for anti-tumor drug development. Utilizing the previously identified hit compound Hit-063 as a starting point and guided by the classic HDAC inhibitor pharmacophore model, a series of novel compounds incorporating an N-benzyl-2-(aryl/heteroaryl)acetamide fragment were rationally designed and synthesized. Among these analogs, compound 27 (Cmpd_27) was identified as the most promising lead, exhibiting potent nanomolar inhibition against HDAC6 with an IC value of 4.29 ± 0.12 nM. Notably, Cmpd_27 demonstrated superior isoform selectivity, with selectivity indices exceeding 150-fold over HDAC1 and HDAC3, as further validated by Western blot analysis. At the cellular level, Cmpd_27 triggered G2/M phase arrest and induced apoptosis in HCT-116 cells, leading to a significant suppression of cell proliferation (IC = 0.69 ± 0.04 μM). Moreover, insights derived from quantum chemical analysis of frontier molecular orbitals and molecular dynamics (MD) simulations provide a robust theoretical foundation for the rational design and structural optimization of next-generation selective HDAC6 inhibitors. - Source: PubMed
Publication date: 2026/08/22
Li TingtingWei LingfangShi HeYan WenyingSun YujieZhang YushaWang YitengLu XiangyuFu YanLiu ZhaoboYuan PingfanLiu JieZhang YangJia QingzhongLi Xuedong - Calcitonin gene-related peptide (CGRP), encoded by the gene, plays a central role in migraine pathophysiology; however, it remains unclear whether migraine is associated with persistent systemic molecular alterations affecting the CGRP pathway during the interictal phase. Transient receptor potential cation channel subfamily A member 1 (TRPA1) stimulates the release of CGRP from nerve endings. We investigated gene-specific and global epigenetic regulatory mechanisms associated with and expression in the peripheral blood of 56 patients with episodic migraine in the interictal phase and 36 headache-free controls. Expression of , , and genes encoding epigenetic regulators, histone deacetylases 1 and 6 (HDAC1 and HDAC6), was assessed by quantitative real-time PCR. DNA methylation of and was evaluated using methylation-specific PCR. Expression of other epigenetic regulators miRNA-375, miRNA-382, and miRNA-34a was determined using TaqMan MicroRNA assays. No significant differences were observed between migraine patients and controls in or expression, nor in DNA methylation of these genes. Similarly, no differences were found in the expression of miRNA-375 and miRNA-382. In contrast, miRNA-34a expression was significantly reduced in migraine patients. Moreover, the expression of and was significantly decreased in migraine. Despite the established role of CGRP in migraine, no evidence of persistent systemic dysregulation of or was detected in peripheral blood during the interictal phase. However, altered expression of miRNA-34a, , and suggests the presence of broader epigenetic and post-transcriptional regulatory disturbances. These findings support a model in which migraine is associated with dysregulation of regulatory mechanisms rather than stable alterations of individual target genes. - Source: PubMed
Publication date: 2026/08/11
Fila MichalKołacz-Milewska KingaGrygiel MałgorzataPrzysło LukaszTworek KarolinaRobaszkiewicz AgnieszkaIonov MaksimBlasiak Janusz - Endothelial apoptosis is a central event in atherosclerotic vascular injury, yet the contribution of the INO80 chromatin-remodeling subunit INO80E to this process remains unclear. This study examined whether INO80E is altered during atherosclerosis (AS)-associated endothelial injury and explored its functional role in ox-LDL-triggered apoptosis. - Source: PubMed
Publication date: 2026/08/12
Liu TingtingLuo QuanyeYang ShihongYang DongmeiLv XuzhenZhao LiyanTuo Qinhui