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
- This chapter presents a comprehensive quantitative framework for identifying and evaluating therapeutic targets for -globin gene disorders through detailed modeling of the fetal-to-adult hemoglobin switch. The biological foundations of -thalassemia and related hemoglobinopathies are reviewed, with particular emphasis on the regulatory network governing - to -globin gene expression. A hybrid Petri net methodology is applied to capture the dynamics of transcriptional regulators, chromatin-remodeling complexes, and globin gene interactions. Both targeted drug-based and RNAi-mediated gene-therapy strategies are examined through computer simulations. Model calibration and validation are performed using available qPCR and RT-qPCR data for key regulators, enabling reliable estimation of kinetic parameters and prediction of treatment outcomes. Comparative analyses of existing interventions identify MS-275 and ACY-957 as the most effective drug-based inducers of -globin, while CHD4-targeting RNAi emerges as the most potent among established gene therapies. The modeling framework further predicts two novel therapeutic strategies: inhibition of the erythroid transcription factor complex as a drug target, and combined silencing of BCL11A, FOG1, and HDAC1/2 as RNAi-mediated gene-therapy approach. Both strategies produce significantly greater -globin induction than currently known treatments. Overall, the chapter demonstrates how hybrid PNs can serve as a powerful computational tool for mechanistically guided target discovery in -globin disorders and related genetic diseases. - Source: PubMed
Bashirov Rza - Growth factor-independent-1 transcription repressor (GFI1) is crucial for determining the differentiation and fate of exhausted CD8 T cells and affects immunotherapy outcomes. However, the effects of tumor cell-intrinsic GFI1 on antitumor immunity and the response to immunotherapy remain unknown. - Source: PubMed
Publication date: 2026/05/22
Xi YuXiao KeweiMeng KelinYu TaiyanWang TianlaiWang XuPan OunanZeng ChenxiWang XueFu XiangningLi Lequn - The objective of this research is to evaluate the diagnostic and prognostic significance of lncRNA PAX8-AS1 in sepsis, and explore its function in regulating the inflammatory response at the molecular level. - Source: PubMed
Publication date: 2026/05/19
Chen QiZhang ErhongZhang YuanCheng MengLiu Fangning - Limited treatment options and poor prognosis create a need for new therapies for triplenegative breast cancer. Modulating lysine acetylation of histone and non-histone proteins via histone deacetylase inhibitors is a promising strategy in cancer therapy. This study aimed to design, synthesize, and test novel panHDAC inhibitors in vitro, building on our previous research. - Source: PubMed
Publication date: 2026/05/11
Dizdarevic SehijaRuzic DusanSrdic-Radic TatjanaVujić Zorica - Alzheimer's disease (AD) is a multifactorial disease with mixed pathologies. Consequentially, drugs targeting multiple pathological processes may offer synergistic benefits. While histone deacetylase (HDAC) inhibitors have demonstrated efficacy in alleviating AD-related pathologies in animal models, the neuroprotective Wnt/β-catenin signaling pathway remains compromised in AD brain. CI-994 is a class I HDAC inhibitor containing N-(2-aminophenyl)-benzamide. Our recent studies indicate that CI-994 is also an activator of Wnt/β-catenin signaling by stabilizing Wnt co-receptor LRP6. We herein use CI-994 as a scaffold to develop novel potent dual modulators of class I HDACs and Wnt/β-catenin signaling for AD therapy. Our lead compound, W2A-28, selectively inhibits class I HDAC1, 2 and 3 with IC values of 0.51 μM, 0.68 μM, and 0.22 μM, respectively, and shows no inhibitory activities on other HDACs. Furthermore, W2A-28 potently activates Wnt reporter activity with an EC value of 1.61 μM in Wnt-3A-expressing HEK293 cells. As expected, activation of Wnt/β-catenin signaling by W2A-28 is associated with elevated LRP6 protein level. Importantly, W2A-28 displays excellent microsomal stability in both mouse and human liver microsomal stability assays, alongside high permeability and a lack of active efflux in MDR1-MDCKII models. Critically, W2A-28 treatment significantly enhances histone acetylation, activates Wnt/β-catenin signaling, and suppresses tau phosphorylation in AD patient-specific cerebral organoids carrying ε4/ε4 or ε3/ε4 with M146V mutation. Our findings position W2A-28 as a promising multi-target drug candidate for AD therapy. - Source: PubMed
Publication date: 2026/05/05
Lu WenyanCaulfield Thomas RLee EunmiJeevaratnam SurenWang NiBu GuojunKanekiyo TakahisaLi Yonghe