ArticleNature communications2018
The protective role of DOT1L in UV-induced melanomagenesis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 82 citations in OpenAlex.
- Epigenetics of Malignant Melanoma: Mechanisms, Diagnostic Approaches and Therapeutic Applications.Oncology research · 2026Review
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- Variant ranking pipeline for complex familial disorders.Scientific reports · 2024Article
- Mutation rate heterogeneity at the sub-gene scale due to local DNA hypomethylation.Nucleic acids research · 2024Article
- DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024Review
- Mi-2β promotes immune evasion in melanoma by activating EZH2 methylation.Nature communications · 2024Article
- An emerging maestro of immune regulation: how DOT1L orchestrates the harmonies of the immune system.Frontiers in immunology · 2024Review
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- SkinNet-INIO: Multiclass Skin Lesion Localization and Classification Using Fusion-Assisted Deep Neural Networks and Improved Nature-Inspired Optimization Algorithm.Diagnostics (Basel, Switzerland) · 2023Article
- Histone post-translational modification and the DNA damage response.Genes & diseases · 2023Review
- DOT1L regulates chromatin reorganization and gene expression during sperm differentiation.EMBO reports · 2023Article
- Gain-of-function mutations in the catalytic domain ofScience advances · 2023Article
- AMPK Phosphorylates ZDHHC13 to Increase MC1R Activity and Suppress Melanomagenesis.Cancer research · 2023Article
- Novel insights into histone lysine methyltransferases in cancer therapy: From epigenetic regulation to selective drugs.Journal of pharmaceutical analysis · 2023Review
- Common and distinct functions of mouse Dot1l in the regulation of endothelial transcriptome.Frontiers in cell and developmental biology · 2023Article
- Set2 histone methyltransferase regulates transcription coupled-nucleotide excision repair in yeast.PLoS genetics · 2022Article
- Histone Methyltransferase DOT1L as a Promising Epigenetic Target for Treatment of Solid Tumors.Frontiers in genetics · 2022Review
- Epigenetic Regulation of Nucleotide Excision Repair.Frontiers in cell and developmental biology · 2022Review
- Signal pathways of melanoma and targeted therapy.Signal transduction and targeted therapy · 2021Review
- Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes.Cellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
30 authors at 18 institutions in 5 countries.
Funding
Abstract
The DOT1L histone H3 lysine 79 (H3K79) methyltransferase plays an oncogenic role in MLL-rearranged leukemogenesis. Here, we demonstrate that, in contrast to MLL-rearranged leukemia, DOT1L plays a protective role in ultraviolet radiation (UVR)-induced melanoma development. Specifically, the DOT1L gene is located in a frequently deleted region and undergoes somatic mutation in human melanoma. Specific mutations functionally compromise DOT1L methyltransferase enzyme activity leading to reduced H3K79 methylation. Importantly, in the absence of DOT1L, UVR-induced DNA damage is inefficiently repaired, so that DOT1L loss promotes melanoma development in mice after exposure to UVR. Mechanistically, DOT1L facilitates DNA damage repair, with DOT1L-methylated H3K79 involvement in binding and recruiting XPC to the DNA damage site for nucleotide excision repair (NER). This study indicates that DOT1L plays a protective role in UVR-induced melanomagenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.