Evidence map›Paper›PMID 24392144›Full record

ArticlePloS one2014

Metabolomics reveals a role for the chromatin-binding protein HMGN5 in glutathione metabolism.

Eric D Ciappio, Kristopher W Krausz, Mark Rochman, Takashi Furusawa, Jessica A Bonzo, Lino Tessarollo, Frank J Gonzalez, Michael Bustin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Biological Functions of HMGN Chromosomal Proteins.International journal of molecular sciences · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

8 authors at 3 institutions in 1 country.

Eric D CiappioLaboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Kristopher W KrauszLaboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Mark RochmanLaboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Takashi FurusawaLaboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Jessica A BonzoLaboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Lino TessarolloNeural Development Section, Mouse Cancer Genetics Program, National Cancer Institute, Frederick, Maryland, United States of America.
Frank J GonzalezLaboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Michael BustinLaboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
National Institutes of Health · USNational Cancer Institute · USCancer Genetics (United States) · US

Funding

Chromosomal Proteins and Chromosomal FunctionsZIABC004496 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BUSTIN, MICHAEL · 2009 to 2023
$12.9M
Biological Functions of Chromosomal ProteinsZIABC011154 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BUSTIN, MICHAEL · 2009 to 2023
$11.0M
Intramural NIH HHS
6 · The paper itself

Abstract

High mobility group nucleosome-binding protein 5 (HMGN5) is a chromatin architectural protein that binds specifically to nucleosomes and reduces the compaction of the chromatin fiber. The protein is present in most vertebrate tissues however the physiological function of this protein is unknown. To examine the function of HMGN5 in vivo, mice lacking the nucleosome-binding domain of HMGN5 were generated and characterized. Serological analysis revealed that compared to wild-type littermates (Hmgn5(+/Y)), mice with a targeted mutation in the HMGN5 gene (Hmgn5(tm1/Y)), had elevated serum albumin, non-HDL cholesterol, triglycerides, and alanine transaminase, suggesting mild hepatic abnormalities. Metabolomics analysis of liver extracts and urine revealed clear differences in metabolites between Hmgn5(tm1/Y) and their Hmgn5(+/Y) littermates. Hmgn5(tm1/Y) mice had a significant increase in hepatic glutathione levels and decreased urinary concentrations of betaine, phenylacetylglycine, and creatine, all of which are metabolically related to the glutathione precursor glycine. Microarray and qPCR analysis revealed that expression of two genes affecting glutathione metabolism, glutathione peroxidase 6 (Gpx6) and hexokinase 1 (Hk1), was significantly decreased in Hmgn5(tm1/Y) mouse liver tissue. Analysis of chromatin structure by DNase I digestion revealed alterations in the chromatin structure of these genes in the livers of Hmgn5(tm1/Y) mice. Thus, functional loss of HMGN5 leads to changes in transcription of Gpx6 and Hk1 that alter glutathione metabolism.

Indexed as

MetabolomicsAnimalsChromatinFemaleGene Expression RegulationGene OrderGene TargetingGlutathioneGlutathione PeroxidaseHexokinaseHMGN ProteinsLiverLiver Function TestsMaleMetabolomeMiceChromatinGlutathioneGlutathione PeroxidaseHexokinaseHK1 protein, mouseHmgn5 protein, mouseHMGN Proteins

Identifiers

PMID24392144
PMCPMC3879345
OpenAlexW2029136419

What OpenQuestion holds

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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.