ArticleeLife2022
EHMT2 methyltransferase governs cell identity in the lung and is required for KRAS
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Loss of EHMT2 enhances NK cell-driven anti-tumor immunity through TGF-β1 suppression.EMBO molecular medicine · 2026Article
- Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer.Journal of translational medicine · 2024Review
- The Role and Mechanism of the Histone Methyltransferase G9a in Tumors: Update.OncoTargets and therapy · 2024Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung development, integrity and repair rely on precise Wnt signaling, which is corrupted in diverse diseases, including cancer. Here, we discover that EHMT2 methyltransferase regulates Wnt signaling in the lung by controlling the transcriptional activity of chromatin-bound β-catenin, through a non-histone substrate in mouse lung. Inhibition of EHMT2 induces transcriptional, morphologic, and molecular changes consistent with alveolar type 2 (AT2) lineage commitment. Mechanistically, EHMT2 activity functions to support regenerative properties of Kras
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Registered trials
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