DNMT3A Assay kit
- Known as:
- DNMT3A Assay reagent
- Catalog number:
- 52033
- Product Quantity:
- 100 reactions
- Category:
- Peptides
- Supplier:
- BPS Bioscience
- Gene target:
- DNMT3A Assay kit
Related genes to: DNMT3A Assay kit
- Gene:
- DNMT3A NIH gene
- Name:
- DNA methyltransferase 3 alpha
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-15
- Date modifiied:
- 2019-04-23
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- The comorbidity of chronic pain and associated negative emotion significantly worsens pain experience and pain chronicity, presenting a severe clinical problem. Despite extensive pre-clinical and clinical studies, the molecular mechanisms underlying the pain-negative-emotion comorbidity are still poorly understood. In this study, we explored an epigenetic mechanism for chronic-pain-induced negative emotion, focusing on the DNA methyltransferase 3a (Dnmt3a) in mice with chronic neuropathic pain. In the parabrachial nucleus (PBN), a brainstem gateway to transmitting pain signals from the peripheral to the brain, we found that chronic pain lasting one month induced anxiety- and depression-like behaviors and downregulated Dnmt3a protein. Overexpression of PBN Dnmt3a rescued the chronic pain mice from developing these behaviors of negative emotion, while knockdown of PBN Dnmt3a was sufficient to induce anxiety-like behavior in naive mice. In contrast, chronic pain increased expression of GluA1-pSer831 subunits of glutamate AMPA receptors in PBN. Dnmt3a knockdown increased both the expression of PBN GluA1-pSer831 and synaptic function of AMPA receptors in PBN neurons. Overexpression of PBN GluA1 induced anxiety-like behavior in naïve mice, whereas knockdown of PBN GluA1 produced an anxiolytic effect and prevented chronic-pain-induced anxiety-like behavior. These results suggest Dnmt3a as a key epigenetic modulator linking chronic pain to negative emotion behaviors through PBN, and PBN GluA1 as an important regulation target of Dnmt3a in the process. - Source: PubMed
Publication date: 2026/07/21
Ge JianlongCai YouqingPan Zhizhong Z - Cadmium (Cd), a bioaccumulative toxic heavy metal, poses a growing concern for offspring reproductive health following gestational exposure. Premature ovarian insufficiency (POI), a major cause of female infertility, remained poorly understood in terms of environmental etiology. This study investigated whether gestational Cd exposure induced ovarian functional decline via epigenetic mechanisms in mice. Using a mouse model of maternal Cd exposure via drinking water, we found that gestational Cd exposure led to POI-like ovarian dysfunction in adult offspring, characterized by diminished ovarian reserve, disrupted estrous cycles, altered serum hormone profiles, and accelerated ovarian aging with fibrosis and DNA damage. Mechanistically, Cd exposure upregulated DNMT1 and DNMT3A expression in offspring ovaries, promoting hypermethylation of the Klotho (Kl) promoter and suppressing its expression. Kl downregulation subsequently attenuated its inhibition of the p53/p21 pathway, triggering granulosa cell senescence and premature follicular depletion. Importantly, administration of the DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-Aza) during gestation partially reversed these Cd-induced epigenetic modifications and ameliorated the ovarian phenotypes in offspring. Our findings revealed a complete pathway through which gestational Cd exposure promoted ovarian aging via DNMT-mediated Kl silencing and p53/p21 activation. This work provided novel mechanistic insights into environmental reproductive toxicity and identified potential targets for intervention. ENVIRONMENTAL IMPLICATION: Cd is a pervasive environmental toxicant threatening female reproductive health, yet its long-term developmental impacts on offspring ovarian aging remain unclear. This study reveals that gestational Cd exposure epigenetically silences the anti-aging gene Kl via promoter hypermethylation, activating the p53/p21/p16-Rb senescence pathway and triggering POI-like ovarian dysfunction in offspring. Importantly, this epigenetic damage is partially reversible with 5-Aza, offering a potential intervention strategy. These findings provide mechanistic insights into how Cd pollution contributes to rising POI incidence, informing developmental origins of reproductive dysfunction and guiding preventive policies for hazardous material regulation. - Source: PubMed
Publication date: 2026/07/22
Jiang JunyuHe MuranShi HaotianXiong YanyanLi BoYuan ChenxiWang HuaLiu ZhibingXu DexiangZhang Jun - Clonal hematopoiesis (CH), an age-related expansion of somatically mutated hematopoietic clones, is associated with increased risk of severe infections including COVID-19, yet the underlying mechanisms remain unclear. Here, we investigated the impact of Dnmt3a deficiency in a murine model of influenza A virus (IAV) pneumonia. Dnmt3a-deficient mice exhibited increased pulmonary viral burden and reduced neutrophil accumulation in IAV-infected lungs despite comparable circulating neutrophil numbers. Functional analyses of neutrophils showed impaired chemotactic migration in vitro, while maturation, antimicrobial enzyme content, and metabolic capacity were unchanged. Transcriptomic profiling revealed downregulation of pathways involved in chemotaxis, cytokine signaling, and cellular activation, including reduced expression of Cxcr1. Supporting the translational relevance of these findings, proteomic analysis of plasma from individuals with germline DNMT3A mutations (Tatton-Brown-Rahman syndrome) revealed alterations in proteins associated with cell migration and cytoskeletal dynamics. Collectively, our findings demonstrate that Dnmt3a loss compromises innate immune defense by impairing neutrophil migration in a cell-intrinsic manner, leading to ineffective pathogen clearance. This work provides mechanistic insight into how CH-associated mutations contribute to age-associated susceptibility to infection and highlights altered leukocyte trafficking as a potential therapeutic target in aging populations with CH. - Source: PubMed
Publication date: 2026/07/24
Zimmer FriedaIi Daniel E KennedyRedding Spencer LCao RuoqiongWaldvogel Sarah MThatavarty ApoorvaBahoua BryanTran Brandon TMaknojia Arushana AGoodell Margaret ARodriguez AntonyMatatall Katie AKing Katherine Y - Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in comparing the western blot data shown in Figs. 2B and 4B, a strong similarity was noted comparing the Active‑caspase 3 band in the '6.25' lane of Fig. 2B with the NIRF band in the '6.25' lane of Fig. 4B; moreover, the ICBP87 bands in the 'Control' and '6.25' lanes of Fig. 6B also appeared to be strikingly similar. Finally, a pair of the DNMT1 bands shown for the western blots in Fig. 6B were very similar to a pair of the DNMT3B blots in the same figure part. Following an independent investigation of this paper in the Editorial Office, the concerns raised by the reader were judged to be well‑founded; therefore, the Editor of has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 6544‑6551, 2017; DOI: 10.3892/mmr.2017.7423]. - Source: PubMed
Publication date: 2026/07/24
Lin YunChen WeimingWang ZhihongCai Pengwei - Thrombosis and bleeding events are major causes of morbidity and mortality in patients with myeloproliferative neoplasms (MPN). The contribution of non-driver mutations, in particular mutations in DNMT3A, TET2, and ASXL1 (collectively DTA) to thrombo-hemorrhagic risk remains unclear. - Source: PubMed
Publication date: 2026/07/23
Haran ArnonWasserstrom AvitalVainstein VladimirKazoom RomiShai ElaArad ArielaRoth BatiaBuchman NoaKalish YosefZimran Eran