HDAC2 & HDAC1 Protein Protein Interaction Antibody Pair
- Known as:
- HDAC2 & HDAC1 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0614
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- HDAC2 & HDAC1 Protein Interaction Antibody Pair
Related genes to: HDAC2 & HDAC1 Protein Protein Interaction Antibody Pair
- 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
- 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 & HDAC1 Protein Protein Interaction Antibody Pair
Related articles to: HDAC2 & HDAC1 Protein Protein Interaction Antibody Pair
- Histone deacetylases (HDACs) act as transcriptional repressors and play essential roles in mammalian development. However, data on the expression and subcellular localization of HDACs in the tongue and oral mucosa remain limited. This study aimed to investigate the spatiotemporal expression patterns of HDACs in the mouse tongue and oral mucosa during postnatal development and aging. - Source: PubMed
Publication date: 2026/08/12
Yang ChuboWang JingruWang MingxingLi HuishuKong JiaqiGuo XinruZhan Yuanbo - RhoA-a member of the Rho family of GTPases-critically regulates synaptic plasticity and immune cell function, which have emerged as key mechanisms in schizophrenia pathogenesis. - Source: PubMed
Publication date: 2026/08/08
Khaki MahsaDavoodian Nahid - There are no effective strategies for treating chronic kidney disease (CKD) because of the limited understanding of its complex pathology. Fibrosis commonly develops and expands during CKD progression, making it a plausible therapeutic target against CKD. We have previously reported that kidney disease induces the myofibroblastic transformation of renal interstitial fibroblasts, which produce the erythroid growth factor erythropoietin, thereby promoting fibrosis through the production of extracellular matrix and leading to erythropoietin-deficiency anaemia. Since histone deacetylases (HDACs) govern cellular differentiation status, this study investigated whether HDAC inhibition could ameliorate renal fibrosis through restoring myofibroblasts to fibroblastic cells. - Source: PubMed
Publication date: 2026/07/20
Ishioka HirotakaIwamura YumaKonta YusukeSato KojiKato KoichiroTanaka TetsuhiroNakai TakuSuzuki Norio - The global emergence of multidrug-resistant (MDR) and hypervirulent (hvKp) strains poses a major clinical challenge. Here, we compared representative classical (cKp), MDR-Kp, and hvKp isolates to define host epigenetic responses during infection. At 24 h post-infection (hpi), infection with all three strains induced HDAC2 upregulation and H3K18 deacetylation, with chromatin immunoprecipitation (ChIP) analysis revealing HDAC2 enrichment at the promoter, linking epigenetic remodeling to autophagy suppression. Functionally, cKp and MDR-Kp isolates promoted M1-like macrophage polarization, whereas hvKp isolate induced an immunosuppressive M2-like phenotype associated with enhanced intracellular bacterial survival and elevated expression. gene knockdown reduced intracellular bacterial survival, while pharmacological inhibition using CI994 and SAHA restored autophagy, normalized cytokine responses, enhanced bacterial clearance, and reversed M2-like polarization induced by hvKp-isolate. Collectively, these findings identify HDAC-mediated epigenetic reprogramming as a central mechanism underlying immune evasion during infection and support HDAC inhibition as a potential host-directed therapeutic strategy. - Source: PubMed
Publication date: 2026/07/09
Abhinand KuniyilSony Shima MerinAnil Avandika BPadmakumar SandhyaJaykumar Abhijith PulimoottilThomas Shwetha SusanMenon Arjun MP C Parvathi MohananR V KrishnaKumar Geetha BNair Bipin GBabu PradeeshMadhavan Aravind - 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