ArticleGenome research2015
Functional compensation among HMGN variants modulates the DNase I hypersensitive sites at enhancers.
Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- High-mobility group N proteins are required for regulation of antigen-presentation genes in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Deficiency of HMGN2 enhances antibacterial activity of macrophages by promoting H3 histone modification-mediated CD14/iNOS expression.Frontiers in immunology · 2025Article
- Epigenetic Regulation of Ameloblast Differentiation by HMGN Proteins.Journal of dental research · 2024Article
- Epigenetic regulation of white adipose tissue plasticity and energy metabolism by nucleosome binding HMGN proteins.Nature communications · 2022Article
- Multiple epigenetic factors co-localize with HMGN proteins in A-compartment chromatin.Epigenetics & chromatin · 2022Article
- H3K27ac nucleosomes facilitate HMGN localization at regulatory sites to modulate chromatin binding of transcription factors.Communications biology · 2022Article
- Human HMGN1 and HMGN2 are not required for transcription-coupled DNA repair.Scientific reports · 2020Article
- High-mobility group nucleosomal binding domain 2 protects against microcephaly by maintaining global chromatin accessibility during corticogenesis.The Journal of biological chemistry · 2020Article
- Biological Functions of HMGN Chromosomal Proteins.International journal of molecular sciences · 2020Review
- Maintenance of active chromatin states by HMGN2 is required for stem cell identity in a pluripotent stem cell model.Epigenetics & chromatin · 2019Article
- Unveiling the gene regulatory landscape in diseases through the identification of DNase I-hypersensitive sites.Biomedical reports · 2019Article
- Epigenetic regulation of REX1 expression and chromatin binding specificity by HMGNs.Nucleic acids research · 2019Article
- Binding of HMGN proteins to cell specific enhancers stabilizes cell identity.Nature communications · 2018Article
- Trisomy of a Down Syndrome Critical Region Globally Amplifies Transcription via HMGN1 Overexpression.Cell reports · 2018Article
- Prediction and identification of transcriptional regulatory elements at the lung cancer-specificOncology letters · 2018Article
- HMGN1 and 2 remodel core and linker histone tail domains within chromatin.Nucleic acids research · 2017Article
- Interplay between H1 and HMGN epigenetically regulates OLIG1&2 expression and oligodendrocyte differentiation.Nucleic acids research · 2017Article
- Elevated HMGN4 expression potentiates thyroid tumorigenesis.Carcinogenesis · 2017Article
- Histone H1 and Chromosomal Protein HMGN2 Regulate Prolactin-induced STAT5 Transcription Factor Recruitment and Function in Breast Cancer Cells.The Journal of biological chemistry · 2017Article
- Nucleosome fragility is associated with future transcriptional response to developmental cues and stress in C. elegans.Genome research · 2017Article
Corrections and comments
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Authors and funding
24 authors at 7 institutions in 2 countries.
Funding
Abstract
DNase I hypersensitive sites (DHSs) are a hallmark of chromatin regions containing regulatory DNA such as enhancers and promoters; however, the factors affecting the establishment and maintenance of these sites are not fully understood. We now show that HMGN1 and HMGN2, nucleosome-binding proteins that are ubiquitously expressed in vertebrate cells, maintain the DHS landscape of mouse embryonic fibroblasts (MEFs) synergistically. Loss of one of these HMGN variants led to a compensatory increase of binding of the remaining variant. Genome-wide mapping of the DHSs in Hmgn1(-/-), Hmgn2(-/-), and Hmgn1(-/-)n2(-/-) MEFs reveals that loss of both, but not a single HMGN variant, leads to significant remodeling of the DHS landscape, especially at enhancer regions marked by H3K4me1 and H3K27ac. Loss of HMGN variants affects the induced expression of stress-responsive genes in MEFs, the transcription profiles of several mouse tissues, and leads to altered phenotypes that are not seen in mice lacking only one variant. We conclude that the compensatory binding of HMGN variants to chromatin maintains the DHS landscape, and the transcription fidelity and is necessary to retain wild-type phenotypes. Our study provides insight into mechanisms that maintain regulatory sites in chromatin and into functional compensation among nucleosome binding architectural proteins.
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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.