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Omics · study · 2026

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

Listed in NCBI GEO

CUX1 represses endogenous retroelements leading to an increased inflammatory signature after CUX1 loss.

Description

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.

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Life Sciences
Provenance · 1 source records, 7 field assertions
SourceKeyLast seenRaw
NCBI GEOGSE29814715 d agoJSON v1
FieldAssertionExtractorEvidence
access_levelsource · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[field].local:field:life-sciencesmapping · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[method].geo_series_type:genome-binding-occupancy-profiling-by-high-throughput-sequencingsource · NCBI GEOconnector:ncbi_geo@1.0.0/gdstype
concepts[organism].NCBITaxon:9606source · NCBI GEOconnector:ncbi_geo@1.0.0/taxon
descriptionsource · NCBI GEOconnector:ncbi_geo@1.0.0/summary
publication_datesource · NCBI GEOconnector:ncbi_geo@1.0.0
titlesource · NCBI GEOconnector:ncbi_geo@1.0.0/title