Evidence map›Paper›PMID 31831052›Full record

ArticleEpigenetics & chromatin2019

Maintenance of active chromatin states by HMGN2 is required for stem cell identity in a pluripotent stem cell model.

Sylvia Garza-Manero, Abdulmajeed Abdulghani A Sindi, Gokula Mohan, Ohoud Rehbini, Valentine H M Jeantet, Mariarca Bailo, Faeezah Abdul Latif, Maureen P West, Ross Gurden, Lauren Finlayson and 3 more

Open access · goldAbstract read
In one paragraph

Article in Epigenetics & chromatin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. H3K27ac Is Essential for Human Naive Pluripotency Modulated by m6A-Driven EP300 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Mitigating Cell Cycle Effects in Multi-Omics Data: Solutions and Analytical Frameworks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  16. Article
  17. Biological Functions of HMGN Chromosomal Proteins.International journal of molecular sciences · 2020
    Review
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 3 countries.

Sylvia Garza-ManeroInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Abdulmajeed Abdulghani A SindiInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Gokula MohanInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Ohoud RehbiniInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Valentine H M JeantetInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Mariarca BailoInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Faeezah Abdul LatifInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Maureen P WestInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Ross GurdenInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Lauren FinlaysonInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Silvija SvambaryteInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Adam G WestInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK.
Katherine L WestInstitute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow, G12 8QQ, UK. katherine.west@glasgow.ac.uk.ORCID 0000-0002-5994-8969
University of Glasgow · GBAl Baha University · SAUniversity of Malaya · MY

Funding

Biotechnology and Biological Sciences Research Council BB/J008605/1Medical Research Council MR/K501335/1Wellcome TrustWellcome Trust ISSF
6 · The paper itself

Abstract

backgroundMembers of the HMGN protein family modulate chromatin structure and influence epigenetic modifications. HMGN1 and HMGN2 are highly expressed during early development and in the neural stem/progenitor cells of the developing and adult brain. Here, we investigate whether HMGN proteins contribute to the chromatin plasticity and epigenetic regulation that is essential for maintaining pluripotency in stem cells.

resultsWe show that loss of Hmgn1 or Hmgn2 in pluripotent embryonal carcinoma cells leads to increased levels of spontaneous neuronal differentiation. This is accompanied by the loss of pluripotency markers Nanog and Ssea1, and increased expression of the pro-neural transcription factors Neurog1 and Ascl1. Neural stem cells derived from these Hmgn-knockout lines also show increased spontaneous neuronal differentiation and Neurog1 expression. The loss of HMGN2 leads to a global reduction in H3K9 acetylation, and disrupts the profile of H3K4me3, H3K9ac, H3K27ac and H3K122ac at the Nanog and Oct4 loci. At endodermal/mesodermal genes, Hmgn2-knockout cells show a switch from a bivalent to a repressive chromatin configuration. However, at neuronal lineage genes whose expression is increased, no epigenetic changes are observed and their bivalent states are retained following the loss of HMGN2.

conclusionsWe conclude that HMGN1 and HMGN2 maintain the identity of pluripotent embryonal carcinoma cells by optimising the pluripotency transcription factor network and protecting the cells from precocious differentiation. Our evidence suggests that HMGN2 regulates active and bivalent genes by promoting an epigenetic landscape of active histone modifications at promoters and enhancers.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationCell Line, TumorCell Self RenewalChromatinHistonesHMGN1 ProteinHMGN2 ProteinMiceNanog Homeobox ProteinNerve Tissue ProteinsNeural Stem CellsNeuronsOctamer Transcription Factor-3Pluripotent Stem CellsBasic Helix-Loop-Helix ProteinsChromatinHistonesHMGN1 ProteinHMGN2 ProteinNanog Homeobox ProteinNerve Tissue ProteinsNeurog1 protein, mouseOctamer Transcription Factor-3Pou5f1 protein, mouseChromatinDifferentiationEmbryonal carcinoma cellsEpigeneticsHMGNNeuronalStem cells

Identifiers

PMID31831052
PMCPMC6907237
OpenAlexW2996548352

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.