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Reduction of di-methyl histone H3K9 (H3K9me2) in CUX1-deficient cells.

GSE298147 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2026/03/11 Platform GPL18573
Summary
CUX1 represses endogenous retroelements leading to an increased inflammatory signature after CUX1 loss. CUX1 interacts with the histone H3K9 methyltransferase, EHMT2 (G9a). EHMT2, in turn, represses endogenous retroelements (EREs) via the deposition of H3K9me2. CUX1-deficient K562 cells exhibited a broad reduction in H3K9me2 deposition, with particularly marked losses at LINEs, SINEs, and LTRs, supporting the model that CUX1 represses ERE expression through EHMT2-mediated H3K9me2 deposition.
Published in
CUX1 restrains latent hematopoietic stem cell plasticity by suppressing stem cell-intrinsic inflammatory pathways
Martinez TC, Jotte MRM, Khan S et al. · Blood 2025 · PMID 40920873 · doi:10.1182/blood.2024026815
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Also filed as BioProject PRJNA1268428 and SRA study SRP588097. Searching any of these in the dataset finder brings you back here.

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