Polyclonal HDAC1
- Known as:
- Polyclonal HDAC1
- Catalog number:
- pc-361
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal HDAC1
Related genes to: Polyclonal HDAC1
- 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: Polyclonal HDAC1
Related articles to: Polyclonal HDAC1
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial hyperplasia, inflammatory cell infiltration, and pathological angiogenesis, ultimately leading to progressive joint damage. Cold-inducible RNA-binding protein (CIRP) has been implicated in inflammatory responses; however, its role in RA-associated angiogenesis remains unclear. In this study, we demonstrate that CIRP gene knockout or pharmacological inhibition using C23 significantly attenuates arthritis severity and reduces synovial angiogenesis in adjuvant-induced arthritis models. In vitro experiments revealed that CIRP promotes human umbilical vein endothelial cell (HUVEC) tube formation, migration, and invasion by upregulating the expression of C-X-C motif chemokine receptor 4 (CXCR4) and Delta-like ligand 4 (DLL4). Notably, blocking extracellular CIRP with C23 inhibited CIRP-induced angiogenesis in HUVECs. Further investigations showed that Toll-like receptor 4 (TLR4) knockdown suppressed CIRP-induced angiogenesis in HUVECs, indicating that CIRP promotes angiogenesis through a TLR4-dependent mechanism. Subsequent mechanistic studies revealed that CIRP upregulates histone deacetylase 1 (HDAC1) expression via TLR4 in HUVECs. We therefore investigated the role of HDAC1 in CIRP-induced angiogenesis, and found that HDAC1 knockdown significantly inhibited this process. Moreover, CIRP promotes pyruvate kinase M2 (PKM2) nuclear translocation and suppresses PKM2 lactylation through the TLR4-mediated HDAC1 pathway. Furthermore, The PKM2 lysine 62 to arginine (K62R) mutant enhances PKM2 nuclear translocation and promotes angiogenesis. Taken together, these results suggest that HDAC1-mediated PKM2 delactylation modification regulates CIRP-induced angiogenesis in RA. - Source: PubMed
Publication date: 2026/07/17
Yao FengYu QiuxiaHu ZhongyaoYan ShuangjingTong HaiyangZheng YanminLi DongshengHu WeirongFang YilongWei XinWang KeZhao YingjieZhou RenpengHu Wei - 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 - 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