Ask about this productRelated genes to: HDAC2 antibody
- Gene:
- HDAC2 NIH gene
- Name:
- histone deacetylase 2
- Previous symbol:
- -
- Synonyms:
- RPD3, YAF1, KDAC2
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2019-02-19
Related products to: HDAC2 antibody
Related articles to: HDAC2 antibody
- Gastrodia elata Blume (G. elata) is a valuable traditional Chinese medicine (TCM) that has been widely used in China. We systematically reviewed tonic and life-extending records in ancient medical literature, as well as the life-prolonging and senescence-delaying effects identified in modern pharmacological research, to provide a theoretical basis for the clinical application and product development of G. elata in tonification and anti-aging. Scientific databases, including CNKI (Chinese literature) and PubMed, were searched to gather relevant literature on the anti-aging effects of G. elata. The targets of the main chemical components of G. elata were predicted and collected through a database, and the intersection of compound targets and disease targets was identified. Protein-protein interaction network analysis, Gene Ontology enrichment, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to explore the potential mechanisms underlying the anti-aging effects of G. elata. The record of G. elata demonstrates a definitive life-extending effect. Modern pharmacological studies have confirmed that it prolongs the lifespan of short-lived animals and slows the aging processes of the brain, skin, bone, and skeletal muscle in animals. Network pharmacology analysis identified 15 common targets shared between candidate target genes of G. elata and anti-aging target genes. TP53, ESR1, EP300, SIRT1, STAT3, CCND1, HDAC2, MDM2, PPARG, TNF, and HSP90AA1 were identified as core genes in the protein-protein interaction (PPI) network analysis. KEGG enrichment analysis indicated that the anti-aging mechanisms of G. elata may be associated with chemical receptor activation, insulin resistance, the citric acid cycle, the PPAR signaling pathway, the glucagon signaling pathway, and the thyroid hormone signaling pathway. This article summarizes previous studies and modern research on the anti-aging effects of G. elata, suggesting that it holds significant potential for clinical applications in anti-aging. - Source: PubMed
Publication date: 2026/04/20
Wang RuoyingXin ChenranLiu WencongCheng ZhiqiangZhu HongyanHan Jihong - This study synthesized a series of C2 and N1-substituted benzimidazole hydroxamic acid (6-19) as HDAC inhibitors. Among them, most of 2-aryl(alkyl)benzimidazole hydroxamic acids (11-16) exhibited HDAC6 activity and slight HDAC1 (or HDAC2) activity. In addition, they also showed anti-angiogenic activity and inhibited the growth of tested cancer cells. For instance, compound 13 has a GI of 3.9 μM against EPCs and inhibited the growth of HCT-116, SK-Hep-1, and PC-3 cells with GI values of 1.3, 4.2, and 7.5 μM, respectively. The exact mechanism underlying the anti-angiogenic effects of these compounds remains unknown, though this study gives an insight into how future HDAC inhibitors that aim to target blood vessel formation can be designed. - Source: PubMed
Liu Yi-TingLai Cheng-TaWang Shih-WeiLiu Shan-ChiHwang Yi-LinTsai Yi-ChenLee Chi-YehLai Yu-WeiYen Juei-YuWang Po-ChuanLee Hsueh-Yun - Histone deacetylases (HDACs) have been identified as a class of crucial epigenetic enzymes that are responsible for the removal of acetyl groups from the lysine residues in the amino-terminal tails of histones. Their overexpression is closely associated with cancer growth, progression, and acquisition of therapeutic resistance, etc. Therefore, the treatment of diverse cancers could benefit from HDACs inhibitors, especially hematologic malignancies. Herein, a series of novel hydroxamate derivatives were designed by incorporating a clover-leaf scaffold into the cap region of SAHA to explore additional binding sites and obtain more potent HDACs inhibitors. Modifications on cap region and linker led to the optimal inhibitor 31a. Preliminary evaluation of inhibitory potency against HDAC isoenzymes indicated that it could inhibit several HDAC subtypes, including HDAC1 (IC = 2.4 nM), HDAC2 (IC = 5.8 nM), HDAC3 (IC = 5.2 nM), and HDAC6 (IC = 3.3 nM). Additionally, it displayed moderate to potent in vitro antiproliferative activity against broad spectrum of cancers, especially MV4-11 cells (IC = 0.17 μM). Flow cytometry analysis showed that it could induce remarkable cell apoptosis at the concentration of 3.0 μM. However, no cell cycle arrest was observed at the test concentration. Importantly, novel binding sites which could enhance binding affinity with HDAC1 were first confirmed in this work. In our opinion, they are worth applying in the development of HDACs inhibitors. Overall, this study provides a new structure design for HDACs inhibitors and also offers promising novel HDACs inhibitors with potential antiproliferative activity against several types of cancers. - Source: PubMed
Publication date: 2026/04/22
Quan XizhengChen YumeiMa FangliNi YudieQi Baohui - The continuous failure to account for biological sex is a key impediment to developing effective neuroprotective treatments for ischemic stroke. While epigenetic modulators such as HDAC inhibitors show promise, the mechanisms behind their sexually dimorphic effects are unknown. We present a unique, sex-specific mechanism in which HDAC2 suppression offers substantial resilience to ischemic brain injury by significantly increasing the endogenous oxytocin (OXT) signaling axis. Through integrated in vitro and in vivo models, we show that HDAC2 knockdown not only reduces infarct size and enhances functional recovery, but also does so more effectively in females. We attribute this improved protection to a strong, female-specific increase of OXT and its receptor (OTR). This increased OXT signaling, possibly mediated by estrogen, resulted in significant decreases in apoptosis, neuroinflammation, and oxidative stress. Our findings show that HDAC2 serves as a critical epigenetic brake on a built-in neuroprotective mechanism that, when activated, triggers a therapeutically potent, sex-divergent response. This study sheds light on chemical biology by identifying a druggable epigenetic target that modulates an important neurohormonal circuit. More broadly, it establishes a new paradigm for individualized stroke therapy, shifting away from a one-size-fits-all strategy and toward leveraging innate, sex-specific protective mechanisms to improve treatment efficacy. - Source: PubMed
Publication date: 2026/03/25
Amin NashwaYuan XiaShi ZongjieWu FeiAbbasi Irum NazYang YangYe SuhongYang QiningGeng YuFang Marong - Cellular senescence plays a significant role in age-related conditions like osteoarthritis (OA) and intervertebral disc degeneration, in part due to the accumulation of senescent cells (SCs) in musculoskeletal tissues. Identifying novel therapeutics that can clear SCs is crucial for improving musculoskeletal health in the elderly. The present study aimed to elucidate the changes in Class I histone deacetylases (HDACs) and their role during senescence. All Class I HDACs except HDAC1 were downregulated during senescence in the human TC28a2 immortalized human chondrocyte cell line. Knockdown experiments showed that HDAC1 is essential for maintaining the viability of both non-senescent cells (NSCs) and SCs, while HDAC2 plays a key role in modulating inflammation in part by targeting the NF-κB signaling pathway. Mocetinostat, an HDAC inhibitor, selectively kills senescent TC28a2 cells and primary human knee chondrocytes via apoptosis while not affecting the viability of NSCs. Mocetinostat also affected both inflammation-associated and chondrogenesis-associated genes. Overall, our findings demonstrate a key role of Class I HDACs in regulating chondrocyte survival and ECM gene expression. Mocetinostat holds promise as a senolytic therapeutic for OA and potentially other aging-related musculoskeletal disorders. - Source: PubMed
Publication date: 2026/04/25
Gupta KavyaSwahn HannahLotz Martin K