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
- While significant advances have been made in maintaining stem cell pluripotency, the successful establishment of embryonic stem cells (ESCs) from various animal species in vitro remains challenging. This highlights the need for further optimization of culture conditions. Through compound library screening, we identified Danofloxacin, a small molecule, as a promoter of mouse ESC stemness. Danofloxacin enhances the formation of undifferentiated colonies and the generation of chimeric mice. Mechanistically, it suppresses HDAC1 expression and activity, resulting in increased acetylation of histone H3 at lysines 9 (H3K9ac) and 27 (H3K27ac), which in turn upregulates the expression of Tert and Prdm10. Functional assays revealed that overexpressing Tert or Prdm10 mimics Danofloxacin's effect on ESC self-renewal, whereas knockdown of either gene disrupts this process. Moreover, the elevated levels of H3K9ac and H3K27ac activate the PI3K/AKT and HIF-1α signaling pathways, both of which contribute to the transcriptional upregulation of Tert and Prdm10. These findings offer new insights into the pluripotency regulatory network and propose potential strategies for isolating ESCs from other species in vitro. - Source: PubMed
Publication date: 2026/09/27
Zhang YanJi JunxiangDong BaoxingZhu ZhenhuaLv XuchengChen PengLiu WenqiangZhou MinYe Shou-Dong - Histone deacetylases (HDACs) are epigenetic enzymes linked to several biological functions and diseases. Class I HDACs (HDAC1-3) share high protein sequence and active site similarity. Hydroxamate-based inhibitors, while highly potent, are non-selective with poor pharmacokinetic profile, prompting exploration of alternative zinc-binding groups. The study applied criteria-guided identification of HDAC3 inhibitors with alternative zinc-binding groups following structure-based virtual screening, with a prioritisation of HDAC3-specific binding interactions and bidentate/monodentate interaction with the zinc ion. Metal-focused chemical libraries were screened virtually followed by biochemical assessment of inhibitory activity of the hit compounds and cell cytotoxicity evaluation. Compound a displayed sub-micromolar HDAC3 potency (IC = 0.99 μM) but limited selectivity for HDAC3, whereas compound b showed reduced potency (IC50 = 15 μM) yet possessed HDAC3 preference. Molecular docking suggests that the zinc-binding group of the compounds form bidentate/monodentate metal coordination with the zinc ion and hydrogen bond interaction with Asp170. Compound a showed a high cytotoxicity IC value of 34.5 μM on neuroblastoma cells (IMR-32 cells) and IC on liver (HepG2) cells was >100 μM, while HDAC3 inhibition occurred at sub-micromolar concentrations. Compound b showed HDAC3 inhibitory preference without inducing cytotoxicity on liver and neuroblastoma cells. - Source: PubMed
Publication date: 2026/09/25
Makgoba Thabo BrightonEgieyeh SamuelKapp ErikaJoubert Jacques - Corneal hyperglycemia is associated with epithelial dysfunction characterized by impaired inflammation, oxidative stress, neuropathy and innate immune mechanisms, as observed in diabetic corneal keratopathy. Therefore, the aim of the study was to investigate at cellular level the effects of moderate to severe acute and chronic challenges of glucose on human primary cultures of corneal epithelial cells (CECs). Human CECs (Innoprot, Spain) were exposed to single or repeated 15 mM or 30 mM High Glucose (HG)-supplemented media (CEC Medium containing plain 5 mM glucose), every 2 days from first stimulations and harvested at day 1 (single/acute challenge) or at days 3 and 5 (repeated/chronic challenge). Mannitol was used as osmotic control and cell sustainability were monitored by trypan blue exclusion test and MTT. Conditioned media were subjected to protein analysis while monolayers were processed for relative real-time RT-PCR. Few selected mediators belonging to the inflammatory, complement, innate receptor, oxidative, DNA enzymes and neurotrophic pathways were tested, and protein levels were assayed on selected mediators (IL-6, IL-8, CFH and C5b-9; ELISA). HG exposure induced a time- and concentration-dependent decrease in CEC metabolic activity, without a comparable reduction in cell number. Acute HG exposure promoted an inflammatory response characterized by increased , , and transcripts, together with an early modulation of complement components and increased expression of and (regulators). Chronic HG exposure induced a marked shift toward complement activation, with increased , , , and transcripts and reduced and expression, with a progressive accumulation of CFH and C5b-9 proteins in a positive relationship. Chronic HG also increased IL-6 and IL-8 protein release and induced a coordinated upregulation of , and , particularly at 30 mM HG. Antioxidant, DNA enzymes and neurotrophic pathways were differentially modulated over time, with an early response followed by chronic upregulation and reduction, progressive / expression, and a biphasic / transcriptional profile. Overall, these findings support a proposed biphasic model of the CEC response to hyperglycemia, characterized by an initial adaptive molecular response followed by progressive dysregulation under prolonged exposure. This early molecular profile might represent an adaptive response to acute metabolic stress, although further studies are required to confirm this functional protective significance. - Source: PubMed
Publication date: 2026/09/21
Dinice LuciaBalzamino Bijorn OmarEsposito GrazianaSquitti RosannaDi Zazzo AntonioMicera Alessandra - Risdiplam, a survival motor neuron 2 (SMN2) splicing modifier for pediatric spinal muscular atrophy (SMA), requires a comprehensive real-world safety evaluation. This study analyzed 1059 pediatric adverse event reports from the FDA Adverse Event Reporting System (2020 Q1-2025 Q4) with risdiplam as the primary suspect drug. Female patients slightly predominated, with 50.9% aged 0-5 years. Disproportionality analyses identified 25 positive signals. Infections and infestations, general disorders, and gastrointestinal disorders were most frequent. Pneumonia, pyrexia, diarrhoea, respiratory tract infection, and nasopharyngitis were most commonly reported. Notably, nephrolithiasis emerged as a novel unlabeled signal in pediatric patients (reporting odds ratio = 11.32). Median time-to-onset was 119 days, with approximately one-third of events occurring within 30 days and another one-third after 1 year. The Weibull model revealed that the top 5 most frequently reported PTs and top 5 SOCs all exhibited an early-onset pattern. Network toxicology identified 75 overlapping targets, with CASP3, HDAC1, and PDGFRA as core targets implicated in calcium signaling, mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase-protein kinase B (PI3K-Akt), and apoptosis pathways. Molecular docking confirmed stable binding (- 10.1 to - 8.6 kcal/mol). Risdiplam demonstrates a generally acceptable long-term safety profile in clinical practice, yet vigilant monitoring of respiratory, infectious, gastrointestinal, and renal adverse events remains essential to optimize the benefit-risk balance. - Source: PubMed
Publication date: 2026/09/25
Liu BenZhong JingziZheng QingqingZhou Wei - Mammary gland involution is a tightly coordinated post-lactational remodeling program that restores tissue homeostasis and preserves the capacity of the gland for subsequent lactation. Although this process requires extensive epithelial regression, stromal remodeling, and immune cell recruitment, the mechanisms that prevent premature or excessive involution remain incompletely understood. Here, we examined the role of metastasis-associated protein 1 (MTA1) in regulating mammary gland involution. - Source: PubMed
Publication date: 2026/09/24
Kim Seung-SuLee Sang-HeonJeong CheolheeKwon Hae-MinHwang SewonLim Ga YoungKa Na-LeeLee Mi-Ock