DMAP1 Polyclonal Antibody
- Known as:
- DMAP1 Polyclonal Antibody
- Catalog number:
- a-1011-100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Epigentek inc
- Gene target:
- DMAP1 Polyclonal Antibody
Related genes to: DMAP1 Polyclonal Antibody
- Gene:
- DMAP1 NIH gene
- Name:
- DNA methyltransferase 1 associated protein 1
- Previous symbol:
- -
- Synonyms:
- DNMAP1, FLJ11543, KIAA1425, DNMTAP1, EAF2, MEAF2, SWC4
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-12
- Date modifiied:
- 2016-10-05
Related products to: DMAP1 Polyclonal Antibody
Related articles to: DMAP1 Polyclonal Antibody
- Targeting specific protein-protein interactions, particularly those involving DNA methyltransferases (DNMTs), offers a promising strategy to resensitise glioblastoma multiforme cells to temozolomide. Glioblastoma multiforme is a highly aggressive brain cancer with a poor prognosis. The long-term efficacy of standard treatment, including temozolomide, is limited due to resistance development. Temozolomide resistance, often due to MGMT overexpression owing to global DNA hypomethylation and complex epigenetic regulation, significantly limits its efficacy. Thus, we developed site-specific DNMT1 inhibitors using peptide-based protein complex disruptors. Their design was guided by AlphaFold2 multimer, which provided insights into the interaction domains between DNMT1 and its protein partners. Peptides mimicking these interaction domains were synthesised and evaluated in a glioblastoma multiforme model. Our studies identified a peptide, namely PPDM2203, that specifically disrupts the DNMT1/DMAP1 interaction. This peptide did not induce global DNA hypomethylation but selectively inhibited DNMT1 activity at specific sites. Moreover, this peptide exhibited significant antitumoral properties, including sensibilisation to temozolomide, site-specific DNA methylation inhibition, cell proliferation, invasion and cytotoxicity. Therefore, the use of AlphaFold2 led to a peptide and offers a novel approach to selectively inhibit DNMT1 activity, enhancing the efficacy and specificity of existing DNMT1 inhibitors. This strategy underscores the potential for developing advanced therapeutic agents that minimize the risk of global DNA hypomethylation and its associated oncogenic effects. - Source: PubMed
Publication date: 2026/06/11
Besson Jean-MaximeChavanieu AlainNadaradjane ArulrajCartron Pierre-FrançoisLopez Marie - Chromatin remodeling is a dynamic epigenetic process that alters chromatin structure to gauge gene accessibility, enabling precise spatiotemporal gene expression, with disruptions often underlying neurodevelopmental disorders (NDDs), although the mechanistic underpinning remains incompletely understood. Despite essential roles in chromatin remodeling processes such as DNA methylation, and histone acetylation and deposition, DMAP1 has not been implicated in human disease. We identified 20 individuals from 16 families with a syndromic NDD carrying homozygous or compound heterozygous variants in DMAP1. Neural-specific knockdown of its Drosophila ortholog, dDMAP1, caused pupal lethality, structural defects in the mushroom body (MB), decreased dendrite length, abnormal social behavior and mechanical-induced seizures. Human reference DMAP1 could largely compensate for the loss of dDMAP1 in knockdown flies, whereas patient variants failed to restore or differentially rescued the phenotypes, confirming their pathogenicity with differing severity. Transcriptome profiling of dDMAP1 knockdown fly brains nominated Cbl and SF1 as downstream targets. Their overexpression rescued the aforementioned lethality and MB defects. Finally, a DNA methylation episignature was identified, leading to the molecular diagnosis of an additional patient. Our findings demonstrate that biallelic inactivating variants in DMAP1 cause a syndromic NDD, expanding the short list of recessive disease-causing genes within the epigenetic machinery. - Source: PubMed
Publication date: 2026/06/11
Wang QinSobering Andrew KTirrito ChristianHaghshenas SadeghehHjortshøj Tina DuelundPlatzer KonradRedler SilkeMarch Michael EMatsuoka Leticia SXi HangZoodsma JosiahChen YuanhuaMori MariLeung Marco LCouque NathalieVerloes AlainPouzet AntoineGiesbertz Noor AaSimon Marleen EhYearwood Ashley KAssing Dominique LHsieh Tzung-ChienLi Jing-MeiLevy Michael AKerkhof JenniferMcConkey HaleyRzasa JessicaLauzon-Young CarolynSulaiman Raashda AAbdulwahab FirdousShamseldin Hanan EAlmontashiri Naif AmAfqi ManalVedanarayanan VettaikorumakankavGuillen Sacoto Maria JWentzensen Ingrid MDamseh Nadirah SBirnbaum Rivkavan Ommeren BabethHopman Saskia MjZaki Maha SElmakkawy GehadAfzal ErumKim JiHyeEfthymiou StephanieHoulden HenryNusrat AmbreenToft MathiasAbdullah UzmaIqbal ZafarTerek ShannonAlkuraya Fowzan SBhoj Elizabeth JMaroofian RezaSadikovic BekimHakonarson HakonSong YuanquanLi Dong - Chalkbrood is a fungal disease caused by the infection of honeybee larvae by Ascosphaera apis. Currently, effective methods for controlling chalkbrood are lacking. Fungal non-coding RNAs play a critical role in enhancing infectivity and pathogenicity, making them potential high-efficacy targets for suppressing A. apis infection. Based on full-length transcriptome data comparing spores and mycelium of A. apis, and the midgut of honeybees (Apis mellifera) infected by A. apis, a specifically expressed long non-coding RNA 6140 (lnc6140) in A. apis was identified. The study demonstrated that lnc6140 in A. apis positively regulates ATPase expression through milR5658-x, thereby influencing pathogen infectivity and chalkbrood development. In this study, after A. apis infection, the expression levels of lnc6140, milR5658-x, and ATPase increased over the infection period. Interference with lnc6140 suppressed the expression of genes associated with A. apis infection and proliferation-Chi3, GriF, AdmB, Pkia, Ste11, and Dmap1-and significantly inhibited chalkbrood incidence. Dual-luciferase assays demonstrated that lnc6140 positively regulates the expression of milR5658-x, and milR5658-x positively regulates the expression of ATPase in A. apis. Similarly, reducing the RNA level of milR5658-x also significantly inhibited chalkbrood incidence. Concurrent reduction of lnc6140 and milR5658-x levels suppressed ATPase expression and markedly decreased chalkbrood occurrence. The result indicated that lnc6140 of A. apis plays a key role in pathogen infection by regulating the milR5658-x-ATPase axis. Suppressing lnc6140 and milR5658-x of A. apis may serve as a crucial strategy for reducing chalkbrood incidence. These findings provide new candidate targets for understanding the pathogenic mechanisms of A. apis and for the prevention and control of chalkbrood. - Source: PubMed
Publication date: 2026/05/23
Qiu JianfengWu TaoZhou ShuaiFan NianGan GenchaoLiu ZhitanFu ZhongminGuo RuiChen Dafu - Despite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of lung cancer progression. Functional studies demonstrated that DMAP1 deficiency exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, DMAP1 deficiency causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating IFN signaling-mediated anti-tumor immune response. Clinical data analyses revealed that high DMAP1 expression is associated with a "cold" tumor microenvironment and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1's function in lung cancer development and offer a scientific basis for designing novel treatment approaches. - Source: PubMed
Publication date: 2026/03/29
Huang KanDai XiLi ShuaihuChen YingxueYu YaxinWang LinLiu KunLyu ShuhanLi ChongyangSun YihuaLi Fei - Glycine decarboxylase (GLDC) is overexpressed in multiple tumor types and contributes to tumorigenesis or immune evasion by unclarified mechanisms. Here we report that GLDC is polyubiquitinated at K636 following EGFR activation, which drives GLDC-dependent transcriptional inhibition of MHC-I genes and induces tumor cells to evade CD8 T cell-mediated immunosurveillance. Mechanistically, EGFR activation triggers SRC-mediated FBXL3 phosphorylation at Y306, enabling its interaction with GLDC in nucleus. FBXL3 targets GLDC for K63-linked polyubiquitination, and promotes the interaction of GLDC with SMARCE1/DMAP1 to inhibit STAT1-triggered transcriptional activation, resulting in transcriptional inhibition of downstream MHC-I genes. Phosphorylation of FBXL3 decreases MHC-I levels in tumor cells and inhibits CD8 T cells immunity in tumors. Consistently, inhibitors of SRC improves tumor-specific CD8 T cells functions in TME and sensitizes antitumor effects of anti-PD-1 therapy. Our findings reveal an SRC-FBXL3-GLDC-MHC-I regulatory circuit that underlies CD8 T cells immune evasion, and provide a potential therapeutic target to enhance ICB therapy. - Source: PubMed
Publication date: 2026/02/03
Liu RuiLi Shu