ArticleClinical epigenetics2025
Selective disruption of DNMT1/ELK1 interactions induces DGKI re-expression and promotes temozolomide sensitivity of MGMT
Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- CYP2E1 and CYP2D6 in Anti-Tuberculosis Drug-Induced Liver Injury: Mechanisms, Epigenetic Regulation, and Translational Implications.Clinical and translational science · 2026Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDNA methyltransferase (DNMT) inhibitors are emerging as a promising class of agents for personalized and targeted cancer therapy, particularly in malignancies with limited therapeutic options such as glioblastoma (GB). In GB, the MGMT/DGKI methylation profile serves as a biomarker for stratifying patients by treatment response. Specifically, the MGMT
resultsCurrent DNMT inhibitors lack specificity for glioblastoma relevant methylation profiles, thereby limiting their therapeutic efficacy. To address this challenge, AlphaFold-based protein-protein interaction predictions were integrated with sequential chromatin immunoprecipitation assays and established DNMT1 interactome data. This integrative approach led to the identification of a DNMT1/ELK1 complex as a critical regulator of DGKI methylation. A peptide mimicking the DNMT1/ELK1 interface, designated EXD
conclusionThis study identifies a clinically actionable biomarker (MGMT
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