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
- 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 - The mechanisms underlying colchicine's (COL's) anti-fibrotic effects in idiopathic pulmonary fibrosis (IPF) remain unclear. Ferroptosis-associated redox imbalance and epithelial-mesenchymal transition (EMT) are well-recognized central drivers of IPF progression, yet the upstream regulatory mechanisms linking redox homeostasis to ferroptotic vulnerability remain incompletely elucidated. - Source: PubMed
Publication date: 2026/09/24
Shi LeileiZhan SiyuWang XingkaiHan ShuangyuLu ShujunLi RuohanXie JunjieYang ChangqingAdili MunireZhang HuixinHong Jau-ShyongWang YubaoFeng Jing - Neuropsychiatric conditions such as depression, anxiety, and stress-related disorders are increasingly associated with Polycystic Ovary Syndrome (PCOS). Evidence suggests that these conditions are not only linked to the metabolic features of PCOS but also share common underlying mechanisms, including hormonal imbalance, neuroendocrine dysfunction, chronic inflammation, and epigenetic changes. Epigenetic mechanisms, such as DNA methylation, histone modifications, and non-coding RNAs (ncRNAs) regulation, may act as important links between endocrine abnormalities and changes in brain function. In this review, we summarize current evidence connecting PCOS with psychiatric disorders through disruptions in the hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-adrenal (HPA) axes, neurotransmitter imbalance, and metabolic dysregulation. Altered activity of DNA methyltransferases and locus-specific methylation changes in stress-responsive genes, including FKBP5, have been associated with dysregulated HPA function. Similarly, histone-modifying enzymes such as histone deacetylases (HDAC1/2) and enhancer of zeste homolog 2 contribute to transcriptional changes in genes involved in synaptic plasticity and neuroendocrine regulation under conditions of hyperandrogenism and insulin resistance. In addition, epitranscriptomic regulation via N-methyladenosine (m6A) modification, mediated in part by fat mass and obesity-associated protein (FTO), influences neuronal activity of gonadotropin-releasing hormone and neurotransmitter signaling. Dysregulated ncRNAs, including microRNAs (miR-34a, miR-155, miR-93, and miR-221) and long ncRNAs (XIST, H19, and MALAT1), further connect inflammatory and metabolic disturbances with neuronal function. Therefore, this review links PCOS to psychiatric disorders through alterations in the HPG and HPA axes, neurotransmitter imbalance, metabolic dysfunction, and epigenetic reprogramming. We further propose an integrated neuroendocrine-epigenetic framework to explain psychiatric vulnerability in PCOS and discuss future directions for precision-targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/09/19
Shirasath Kamini RAwathale Sanjay NGoyal Sameer N - The interaction between Astragaloside IV (AS-IV) and the gut microbiota is known to help prevent cardiovascular disease, however, its underlying mechanism through which AS-IV modulates the balance of intestinal flora to ameliorate heart failure (HF) remains unclear. - Source: PubMed
Publication date: 2026/09/16
Shi MinWei JiamingYuan HuiGuo Zhihua