Recombinant Human Histone Deacetylase 2 HDAC2
- Known as:
- Recombinant Human Histone Deacetylase 2 HDAC2
- Catalog number:
- enz-157
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Histone Deacetylase 2 HDAC2
Related genes to: Recombinant Human Histone Deacetylase 2 HDAC2
- 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: Recombinant Human Histone Deacetylase 2 HDAC2
Related articles to: Recombinant Human Histone Deacetylase 2 HDAC2
- Studies have shown that chronic morphine exposure results in altered patterns of gene expression through epigenetic mechanisms, suggesting potential transgenerational effects on the offspring's epigenome. This study investigated transgenerational consequences of maternal pre-pregnancy chronic morphine exposure on offspring anxiety-like behaviors and alterations in epigenetic-related genes miR-96, miR-137, MeCP2 and HDAC2. Adolescent female Wistar rats had access to morphine (0.4 mg/mL) in drinking water (controls: tap water) for 50 days before mating with morphine-naïve males. Offspring underwent the forced swim test (FST) and open field test (OFT) to assess anxiety-like behaviors. Gene expression was analyzed in hippocampus from offspring and ovarian tissue from dams. Offspring from morphine-treated dams exhibited significant increases in floating time (F = 43.5; < .001) and spent time in the center area of the OFT (F = 68.1; < .001). MeCP2 and HDAC2 gene expressions were significantly increased in the ovarian tissue of morphine-treated dams (MeCP2: t = 4.3; < .01; HDAC2 t = 8.6; < .001). In offspring of morphine-treated dams, MeCP2 (F = 37.5; < .001) and HDAC2 (F = 62.6; < .001) expression in the hippocampus was significantly increased, whereas miR-137 (F = 25.5; < .001) and miR-96 (F = 23.8; < .001) expression was significantly decreased. These findings underscore that maternal preconception morphine exposure induces neurobehavioral deficits across generations, likely mediated by epigenetic memory in the maternal germline. This suggests preconception opioid exposure could affect offspring's mental health and stress phenotypes, underscoring the need to integrate screening, counseling, and harm reduction into reproductive and addiction care. - Source: PubMed
Publication date: 2026/06/30
Amri JamalGholami MasoumehSakhaie Mohammad HassanAkbari AhmadSadegh Mehdi - Despite the significant contribution of Antiretroviral Therapy (ART) in the management of viral replication and infection, HIV latency still presents a major barrier to complete eradication. Histone Deacetylases (HDACs), particularly Class I HDACs (the isoforms 1, 2 and 3) have been reported to play a pivotal role in maintaining this latency by contributing to transcriptional silencing. Selective HDAC inhibitors (HDACis) that target these isoforms can reactivate HIV reservoirs, encouraging viral growth and its subsequent recognition by the immune system, thus its clearance from the body. This is known as the "shock and kill" hypothesis. - Source: PubMed
Mugisa SimonMohammed HayiruBursal ErcanMurahari Manikanta - The genetic basis of extreme cognitive plasticity in human innovators remains poorly characterized. Here, we demonstrate that the genomic architecture underlying scientific innovation significantly overlaps with the polygenic risks for neuropsychiatric phenotypes, such as schizophrenia. Utilizing a comparative genomic approach across psychiatric cohorts (PGC) and the UK Biobank (Scientific Creativity), we identify a coordinated "Vanguard Engine" consisting of hyper-tuned voltage-gated calcium channels ( ), glutamatergic receptors ( ), synaptic plasticity regulators ( ), and the core linguistic-symbolic coordinator ( ). We posit that these variants establish a high-voltage neural environment optimized for associative divergence. Furthermore, we characterize the and loci as critical metabolic governors against thermal overload and identify structural variance in as the epigenetic clamp linking ancestral fuel availability (β-hydroxybutyrate) directly to the transcriptional control of this plasticity network. We conclude that psychiatric pathology is an emergent property of a fuel-mismatch, wherein a high-performance cognitive architecture is sustained by a carbohydrate-heavy diet, leading to systemic thermodynamic failure. This framework provides a unified, mechanistic explanation for the spectrum between extreme cognitive innovation and pathological collapse. - Source: PubMed
Publication date: 2026/06/16
Krantz Bryan A - Diffuse midline glioma (DMG) is a lethal pediatric brain tumor, driven by profound epigenetic dysregulation, raising the possibility that targeting epigenetic regulators such as histone deacetylases (HDACs) could provide a therapeutic benefit. However, despite preclinical activity, currently available HDAC inhibitors have shown limited clinical translation due to poor central nervous system (CNS) penetration and a lack of HDAC isoform selectivity. - Source: PubMed
Publication date: 2026/06/25
Groves AndrewKirkland Orville OCascio Costanza LoWang XiuqiHeaslip CalebMarques Joana GracaSong ChenPoetschke RebeccaWang TingjianChin Diana HAsante YawLiu QiKim HyunminGu ShanqingTrissal MariaLabelle JennaCruzeiro Gustavo Alencastro VeigaJones Kristen LCameron Amy BClark Louise MLeeper BrittaneyNguyen Quang-DeGryder Berkley EFilbin Mariella GQi Jun - The DNA damage response (DDR) is critical for pancreatic ductal adenocarcinoma (PDAC) development and therapeutic responses, including to genotoxic agents. While epigenetic modulators have been shown to contribute to the DDR, how chromatin regulation dictates responses to DNA damage in PDAC remains incompletely understood. Here, we identify Class I histone deacetylases (HDACs) as critical regulators of the DDR. HDAC1/2 direct the genomic distribution of H3K27ac, ensuring sufficient BRD4 and RNA polymerase II (Pol II) occupancy at DDR gene promoters. HDAC inhibition by entinostat shifts the balance of H3K27 acetylation preferentially toward intergenic regions, diverting BRD4 and Pol II from promoters, thereby suppressing DDR gene expression. In line with this, HDAC inhibition heightens DNA damage and sensitizes PDAC to diverse DNA-damaging and DDR-targeting agents. Since the clinical development of HDAC inhibitors has been limited by systemic toxicity, we developed bottlebrush prodrug (BPD) nanoparticles for tumor-selective entinostat delivery. Entinostat-BPD achieved tumor-specific HDAC inhibition while displaying potent efficacy and reduced systemic toxicity. These findings reveal an HDAC-dependent DDR vulnerability and offer combinational and precision targeting strategies to facilitate clinical translation and improve PDAC patient outcomes. - Source: PubMed
Publication date: 2026/06/25
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