HDAC2, His, Human
- Known as:
- HDAC2, histidine, Human
- Catalog number:
- Z03028-10
- Product Quantity:
- 10,0ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- HDAC2 His Human
Related genes to: HDAC2, His, Human
- 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, His, Human
Related articles to: HDAC2, His, Human
- Newcastle disease virus (NDV) remains a substantial threat to the worldwide poultry industry. Targeting ion homeostasis is studied as a potential antiviral strategy to prevent viral infection and treat channelopathies. Quinoline derivatives, such as 8-aminoquinolines (AQ), are well-established scaffolds in medicinal chemistry with known antiviral properties. The study introduces a novel series of AQ derivatives and evaluates their transmembrane zinc (Zn²⁺) transport activity. Our results suggested that a potent Zn²⁺ transporter, AQ-CN, effectively suppressed NDV replication post-infection, both in vitro and in ovo, with reduced hemolytic activity and potent inhibitory concentration. Additionally, elevated Zn²⁺ levels affected host epigenetic regulators, downregulating Class I histone deacetylases (HDAC1, HDAC2, HDAC3, HDAC8) and reducing global lysine acetylation. Furthermore, in the presence of Zn, AQ-CN increased type I interferon signaling and upregulated antiviral cytokine genes. Pharmacological inhibition with valproic acid, a class I HDAC inhibitor, largely restored the antiviral phenotype, indicating that HDAC-dependent mechanisms are involved in the observed effect. Overall, our findings point to AQ-CN-mediated transmembrane transport as a viable anti-NDV strategy and support a model in which zinc-regulated host Class I HDAC pathways help combat NDV replication. - Source: PubMed
Publication date: 2026/07/13
Mazumder PriyankaDey SubhasisBhattacharya ShinjiniMohanta Pritam KumarManna DebasisKumar Sachin - Histone deacetylase 2 (HDAC2) critically regulates macrophage inflammatory responses and lipid metabolism, yet its potential as a therapeutic target in atherosclerosis (AS) remains to be fully established. This study investigates the therapeutic effects and molecular mechanisms of HDI-1, a novel selective HDAC2 inhibitor, in AS. Fluorescence affinity assays and molecular docking were employed to assess HDI-1 binding to HDAC2. Histone acetylation, lipid accumulation, and expression of lipid transporters (ABCA1, CD36) were evaluated in PMA-differentiated THP-1 macrophages using Western blot, Oil Red O staining, and immunofluorescence. Reactive oxygen species (ROS) levels and Nrf2/HO-1 pathway activation were also measured. In vivo, the efficacy of HDI-1 was examined in high-fat diet-fed ApoE mice. HDI-1 demonstrated high binding affinity for HDAC2, selectively inhibited its activity, and significantly increased H3K9 and H3K27 acetylation. In macrophages, HDI-1 concentration-dependently reduced ox-LDL uptake and lipid accumulation by upregulating ABCA1 and downregulating CD36. Additionally, HDI-1 activated the Nrf2/HO-1 pathway, suppressed ROS generation, and mitigated oxidative stress. In ApoE mice, HDI-1 treatment attenuated aortic plaque formation and ameliorated associated pathological changes. By selectively targeting HDAC2, HDI-1 coordinately modulates macrophage lipid metabolism and oxidative stress responses, effectively attenuating AS progression. These findings position HDI-1 as a promising therapeutic candidate for AS. - Source: PubMed
Publication date: 2026/07/15
Hu ShashaZhao ChenyangBao YizhongLou JiangjieLv KaiqiWeng Yingzheng - Class I histone deacetylases (HDAC1, HDAC2, HDAC3, and HDAC8) are key chromatin regulators, but how they are activated by chaperonin TRiC remains elusive. Using cryo-electron microscopy, cross-linking mass spectrometry, and biochemistry analyses of tagged HDACs overexpressed in HEK293F cells, we identify class I HDACs as TRiC substrates and elucidate the TRiC-assisted folding pathways of HDAC1 and HDAC3 across ATPase cycle, orchestrated by distinct co-chaperone/cofactor networks. In closed TRiC chamber, both clients adopt near-native conformations and engage similar binding interfaces. In the open state, however, their pathways diverge: HDAC3 involves Hsp70 atop TRiC and PDCD5 within the chamber, whereas HDAC1 involves prefoldin atop TRiC, revealing distinct mechanisms of substrate delivery and folding modulation. We also identify an unexpected bent conformation of CCT4 in TRiC-HDAC1 complex that may relate to co-chaperone release. By contrast, HDAC8 folds independently of TRiC. Together, these findings reveal client-specific co-chaperone/cofactor networks governing TRiC-assisted folding of class I HDACs, shedding light on the sophisticated regulatory landscape of TRiC. - Source: PubMed
Publication date: 2026/07/15
Li ZuyangZhao QiaoyuJiang WanyingSong QianqianZhou XuehaiShi XiangyiZhang QingWang YanxingLin YinghongYin YuePan ChenCong Yao - Chronic exposure to morphine induces oxidative stress and alters the hippocampal expression of genes encoding enzymes involved in epigenetic modifications (e.g., DNA methyltransferases; DNMTs and Histonedeacetylases; HDACs) and apoptosis-related signaling (e.g., Bax and Bcl-2). This study examined the effects of vitamin E and L-carnitine supplementation on cognitive function and hippocampal gene expression following morphine administration in adult male NMRI mice. Morphine was administered subcutaneously twice daily at escalating doses: 10 mg/kg for 10 days, 20 mg/kg from day 10 to 20, and 30 mg/kg from day 20 to 45. Antioxidants (vitamin E at 200 mg/kg, L-carnitine at 100 mg/kg, or both) were administered starting on day 10. Behavioral tests, including the open field test, elevated plus maze, and novel object recognition, were conducted on days 43-45. Hippocampal analyses assessed mRNA expression of DNMT3A, DNMT3B, HDAC1, HDAC2, Bax, and Bcl-2, as well as malondialdehyde (MDA) levels, total antioxidant capacity (TAC), and CA1 Nissl staining. Morphine-treated mice exhibited increased anxiety-like behavior, though this effect was not consistently reversed by antioxidants, and memory impairment compared to saline controls. Antioxidant treatment partially mitigated these behavioral deficits. Biochemically, morphine elevated MDA and reduced TAC levels, while antioxidant administration attenuated these markers toward control levels. Histologically, morphine increased CA1 cellular damage, which was attenuated by antioxidants. At the molecular level, morphine increased Bax mRNA and decreased Bcl2 mRNA expression; antioxidant treatment partially reversed these changes. Morphine also increased DNMT3B mRNA expression, which was reversed by antioxidants. Additionally, HDAC1 and HDAC2 mRNA expression decreased with morphine treatment and was enhanced by vitamin E and L-carnitine. These findings suggest that vitamin E and L-carnitine may attenuate morphine-induced hippocampal dysfunction through modulation of oxidative stress and altered gene expression, supporting their potential as adjunctive therapies for opioid-related cognitive impairment. - Source: PubMed
Publication date: 2026/07/15
Alizadeh MarziehHaghpanah TaherehEzzatabadipour MassoodShamsara AliAfarinesh Mohammad Reza - Colorectal cancer (CRC) is a major cause of cancer-related death due to recurrence and therapeutic resistance. This study evaluates whether combining panobinostat, a histone deacetylase (HDAC) inhibitor, with epigallocatechin gallate (EGCG), a green tea-derived polyphenol, enhances anti-tumor activity through modulation of HDAC expression in CRC cell lines. - Source: PubMed
Publication date: 2026/07/15
Khader Mai KamalAbbas Manal AAl-Kabariti Aya Y