ArticleMolecular cell2009
HMGN proteins act in opposition to ATP-dependent chromatin remodeling factors to restrict nucleosome mobility.
Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 54 citations in OpenAlex.
- The inhibitory effect of hepatic cancer energy metabolism on immune checkpoint therapy: perspectives from single-cell multi-omics analysis.Frontiers in immunology · 2026Article
- Structural basis of nucleosome recognition by the conserved Dsup and HMGN nucleosome-binding motif.Genes & development · 2025Article
- Damage-associated molecular patterns and sensing receptors based molecular subtypes in malignant pleural mesothelioma and implications for immunotherapy.Frontiers in immunology · 2023Article
- The role of auxiliary domains in modulating CHD4 activity suggests mechanistic commonality between enzyme families.Nature communications · 2022Article
- Reconstitution of Chromatin by Stepwise Salt Dialysis.Bio-protocol · 2021Article
- Site-specific modification and segmental isotope labelling of HMGN1 reveals long-range conformational perturbations caused by posttranslational modifications.RSC chemical biology · 2021Article
- Maintenance of active chromatin states by HMGN2 is required for stem cell identity in a pluripotent stem cell model.Epigenetics & chromatin · 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
- Lessons from the Crypt: HMGA1-Amping up Wnt for Stem Cells and Tumor Progression.Cancer research · 2018Review
- A simple and versatile system for the ATP-dependent assembly of chromatin.The Journal of biological chemistry · 2017Article
- HDAC6 Deacetylates HMGN2 to Regulate Stat5a Activity and Breast Cancer Growth.Molecular cancer research : MCR · 2016Article
- HMGN proteins modulate chromatin regulatory sites and gene expression during activation of naïve B cells.Nucleic acids research · 2016Article
- Functional interplay between histone H1 and HMG proteins in chromatin.Biochimica et biophysica acta · 2016Review
- Functional compensation among HMGN variants modulates the DNase I hypersensitive sites at enhancers.Genome research · 2015Article
- Nucleosome structure and function.Chemical reviews · 2015Review
- The high-mobility group nucleosome-binding domain 5 is highly expressed in breast cancer and promotes the proliferation and invasion of breast cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- The tumor suppressor chromodomain helicase DNA-binding protein 5 (CHD5) remodels nucleosomes by unwrapping.The Journal of biological chemistry · 2014Article
- Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 Lys27 trimethylation.Nature genetics · 2014Article
- [Inhibitory effects of high mobility group chromosomal protein N2 on human tongue carcinoma transplanted in nude mice].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The high-mobility group N (HMGN) proteins are abundant nonhistone chromosomal proteins that bind specifically to nucleosomes at two high-affinity sites. Here we report that purified recombinant human HMGN1 (HMG14) and HMGN2 (HMG17) potently repress ATP-dependent chromatin remodeling by four different molecular motor proteins. In contrast, mutant HMGN proteins with double Ser-to-Glu mutations in their nucleosome-binding domains are unable to inhibit chromatin remodeling. The HMGN-mediated repression of chromatin remodeling is reversible and dynamic. With the ACF chromatin remodeling factor, HMGN2 does not directly inhibit the ATPase activity but rather appears to reduce the affinity of the factor to chromatin. These findings suggest that HMGN proteins serve as a counterbalance to the action of the many ATP-dependent chromatin remodeling activities in the nucleus.
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.