HDAC2 antibody - middle region (ARP32619_P050)
- Known as:
- HDAC2 (anti-) - middle region (ARP32619_P050)
- Catalog number:
- arp32619_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HDAC2 antibody - middle region (ARP32619_P050)
Related genes to: HDAC2 antibody - middle region (ARP32619_P050)
- 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 - middle region (ARP32619_P050)
Related articles to: HDAC2 antibody - middle region (ARP32619_P050)
- We employed an integrated bioinformatics screening approach along with Mendelian randomization (MR) analysis to explore potential genetic targets for varicose veins of lower extremities (VVs) and identify potential treatment options for VVs. Differential expression analysis was conducted using R software to identify differentially expressed genes (DEGs) of VVs from the Gene Expression Omnibus database. Weighted gene co-expression network analysis (WGCNA) was performed to identify co-expression networks. Functional enrichment analyses were conducted for the identified genes. A protein-protein interaction network was constructed to analyze the interactions among the identified genes. Additionally, genome-wide association studies data for VVs were downloaded for MR analysis. Various methods, including inverse-variance weighted, were employed to assess potential causal associations with VVs risk, followed by sensitivity analysis. The DEGs identified from the VVs Gene Expression Omnibus dataset included 180 upregulated genes and 335 downregulated genes. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis revealed that the downregulated DEGs were significantly associated with nuclear protein-containing complexes and nucleic acid binding (P < .05). WGCNA highlighted a highly significant "turquoise" module comprising 78 downregulated genes (P = 2e - 04). The protein-protein interaction network analysis of the significant DEGs and the WGCNA "turquoise" module identified 224 nodes and 491 edges, uncovering several hub genes such as BRCA1, NCBP2, GTPBP4, HDAC2, KHDRBS1, and HNRNPR. Detailed functional enrichment analysis indicated involvement in tumor-like cellular proliferation and differentiation processes, including protein acetylation, RNA splicing, and metabolic processes. MR analysis revealed a causal association between the tumor-related gene Ecto-NOX disulfide-thiol exchanger 2 (ENOX2) and the risk of VVs, with a statistical significance (odds ratio: 1.0016; 95% confidence interval: 1.0003-1.0029; P = .015) according to inverse-variance weighted analysis. Sensitivity analysis confirmed the absence of heterogeneity and horizontal pleiotropy in the observed associations (P > .05). "Leave-one-out" validation analysis did not indicate any changes. Our study unveils the involvement of ENOX2 and the related mechanisms in the pathogenesis of VVs, suggesting their potential as genetic targets for treatment. - Source: PubMed
He QiuruiZhang XiaohongTao ChenChen ChenmingYan Weiming - Pancreatic cancer (PC) cells suppress dendritic cell (DC) maturation and function through multiple pathways, further impairing antitumor activity of CD8 T cells. Our previous study revealed that caspase-recruitment domain-containing protein 9 (CARD9) deficiency led to DC dysfunction and exacerbated PC progression, yet the precise mechanism underlying CARD9 downregulation in DCs remains elusive. In this study, we observed that CARD9 expression was progressively downregulated in PC tumors and associated with advanced clinicopathological stages and DC dysfunction. Functionally, PC cells reduced CARD9 expression, impaired DC maturation and weakened CD8 T cell activation, with these suppressive effects attenuated in CARD9-deficient DCs and reversed when CARD9 was restored. Then, we identified YY1 as a critical upstream transcription factor that bound to the promoter of CARD9 and repressed it, accompanied with DC dysfunction and tumor growth. Mechanistically, tumor-derived lactate induced YY1 lactylation at lysine 183, facilitating YY1 nuclear entry and strengthening its combination with CARD9 promoter. Furthermore, we identified p300 as the "writer" catalyzing YY1-K183 lactylation, and HDAC2 as its enzymatic "eraser". Lactylation enhanced YY1 stability by limiting ubiquitination, sustaining YY1 activation and reinforcing CARD9 suppression. Overall, our findings define a lactate-p300/HDAC2-YY1 lactylation-CARD9 regulatory axis that restricts DC function and promotes immune escape in PC. - Source: PubMed
Publication date: 2026/05/01
Ding LingyanTian ChengFeng YitingXu RuochenLi SenlinZheng MengzhuWang XiaoyanXu QianqianXiang Ming - Obesity is a major public health problem and a risk factor for metabolic disorders, including type 2 diabetes and cardiovascular disease. Additionally, accumulating evidence suggests that obesity impairs male reproductive capacity, potentially leading to infertility. However, molecular insights into the effects of obesity on the male reproductive system remain elusive. In this study, we examined the effects of diet-induced obesity on epigenetic marks-specifically histone acetylation-and the expression of epigenetic regulatory enzymes in mouse testes. C57BL/6 N male mice were randomly divided into two groups: a control group fed a control diet (10% kcal from fat) and a diet-induced obesity group fed a high-fat diet (HFD; 45% kcal from fat) for 8 weeks. Then, the acetylated histone H3 (K9 and K14) and histone H4 (K5, K8, K12, and K16) levels, as well as the expression of the histone deacetylase (HDAC) family, were investigated in the testes. We found that chronic HFD exposure decreased the acetylation levels of histone H4, but not histone H3, in the entire testis. We also observed the increased expression of HDAC8 at both the mRNA and protein levels in the testes of HFD-fed mice. HFD exposure did not affect the expression of other class I HDACs (HDAC1, HDAC2, and HDAC3) in the testes. These findings suggest that HFD-induced obesity disrupts epigenetic features in the testes, specifically through the modulation of HDAC8 and histone H4 acetylation, providing novel insight into obesity-induced male reproductive dysfunction. - Source: PubMed
Publication date: 2026/05/20
Aizawa ShuOhno HikariYamamuro Yutaka - Autism Spectrum Disorder (ASD) is a neurodevelopmental condition with a strong genetic basis. Most genetic studies on ASD emphasize de novo mutations, while inherited rare variants remain understudied. We hypothesize that subtle, inherited ASD-related traits accumulate across generations and clinically manifest as ASD in offspring. To investigate this, we extracted inherited variations from trio-based Whole Exome Sequences (WES) of 23 simplex ASD families (accession number PRJNA1071313 and PRJNA1072259). Data was processed in BWA, GATK and VarScan. Variants were annotated, filtered for functional impact, and scored using a 'weighted scoring' approach based on intolerance to genetic alterations. Overall 751 'weighted-genes' with evolutionary and neuronal functions hosting deleterious inherited variations were functionally annotated for ASD-linked behaviours and comorbidities. We found 149 (20%) genes enriched for core ASD-behaviours like social-interaction and restrictive repetitive behaviours (RRB), 200 genes (26.6%) for associated-behaviours like hyperactivity, communication, intelligence and mood and 225 genes displayed neuronal-functions (p = 3.799E-20). Importantly, 62% of RRB genes displayed sensory functions and 71.43% of genes associated to social interaction deficits were also linked to seizures. Brain tissue expression analysis of all 751 genes revealed 95 prenatally and 195 postnatally upregulated genes were enriched with neurodevelopmental and neurotransmission functions, respectively; protein-protein-interactions suggested genes BUB1, HMGA2, HDAC2, KALRN, SORL1, IGF2, FASN, WFS1 as promising new-candidates for ASD. In our ASD cohort, inherited variations in genes regulating sensory function and neurodevelopment were also RRB producing genes- supporting a multigenic, subdued but additive genetic load being passed down from unrelated parents to their offsprings- promising an underexplored avenue for autism genetic research. - Source: PubMed
Publication date: 2026/05/25
RameshRaju Meghana KommerahalliParambath Snijesh ValiyaSrividhya DurbagulaShankarappa BhagyalakshmiBasappa Ramachandra NallurMurthy Ashitha S Niranjana - Chronic methamphetamine (Meth) abuse represents a significant global public health crisis, characterized by profound and often persistent cognitive deficits, particularly in hippocampal-dependent memory and learning. This narrative review synthesizes current evidence on the molecular mechanisms through which chronic Meth exposure disrupts hippocampal synaptic plasticity, ultimately driving cognitive impairment. We establish that the initiating event involves Meth-induced dysregulation of dopaminergic signaling, primarily through dopamine transporter (DAT) inhibition, leading to sustained extracellular dopamine surges. This dopamine excess triggers a pathogenic cascade dominated by three interconnected processes: (1) pronounced oxidative stress via dopamine auto-oxidation and mitochondrial dysfunction, generating reactive oxygen species (ROS) that damage synaptic components; (2) mitochondrial apoptotic activation through p53-Bax signaling, cytochrome c release, and caspase-3-mediated cleavage of synaptic scaffolding proteins (e.g., PSD-95, ARC); and (3) suppression of neurotrophic support via BDNF-TrkB-PI3K/Akt pathway impairment, compounded by glutamate receptor dysregulation (NMDAR internalization, AMPAR trafficking defects). These mechanisms converge to induce structural synaptic pathology-including dendritic spine loss (notably mature mushroom spines in dentate gyrus), presynaptic vesicle depletion, and postsynaptic density disintegration-and functional deficits in LTP and LTD. Critically, these processes are amplified by neuroinflammation (microglial TNF-α/IL-1β release) and epigenetic dysregulation (HDAC2 upregulation, BDNF promoter methylation), creating a self-sustaining cycle of synaptic injury. Preclinical and clinical evidence consistently links these molecular disruptions to measurable cognitive decline, including impaired spatial navigation, pattern separation, and declarative memory. Therapeutic strategies targeting key nodes of this cascade show significant promise: dopamine stabilizers (e.g., aripiprazole) normalize D1/D2 receptor imbalance; anti-apoptotics (e.g., minocycline, resveratrol) inhibit caspase-3 and p53; neurotrophic agents (TrkB agonists, BDNF mimetics) restore synaptic protein synthesis; and antioxidants (e.g., N-acetylcysteine) counteract ROS. Future research must address critical gaps in understanding sex-specific vulnerabilities, circuit-selective susceptibility (e.g., hippocampal-VTA loops), and the role of stable epigenetic modifications in sustaining cognitive deficits. Advancing multi-target therapeutic approaches aligned with the temporal progression of Meth neurotoxicity offers the best hope for reversing synaptic dysfunction and mitigating the enduring cognitive burden of Meth addiction. - Source: PubMed
Publication date: 2026/05/25
Hedayati-Moghadam MahdiyehRazazpour FatemeHakemi ZohrehKhani FatemeBaghcheghi Yousef