Evidence map›Paper›PMID 22192339›Full record

ArticleThe Journal of nutritional biochemistry2012

K16-biotinylated histone H4 is overrepresented in repeat regions and participates in the repression of transcriptionally competent genes in human Jurkat lymphoid cells.

Luisa Rios-Avila, Valerie Pestinger, Janos Zempleni

Abstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Luisa Rios-AvilaDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583-0806, USA.
Valerie Pestinger
Janos Zempleni
University of Nebraska–Lincoln · US

Funding

Vitamin-dependent modifications of histonesR01DK063945 · NIDDK · UNIVERSITY OF NEBRASKA LINCOLN · PI ZEMPLENI, JANOS · 2004 to 2011
$2.3M
Biotin sensing and chromatin remodeling by holocarboxylase synthetaseR01DK077816 · NIDDK · UNIVERSITY OF NEBRASKA LINCOLN · PI ZEMPLENI, JANOS · 2009 to 2011
$861k
Novel histone biotinylation sites and relationships to other epigenetic marksR21DK082476 · NIDDK · UNIVERSITY OF NEBRASKA LINCOLN · PI CHANG, YIE-HWA, EISSENBERG, JOEL C · 2009 to 2010
$535k
Epigenetic effects of biotin on activation of endogenous viral sequencesR21ES015206 · NIEHS · UNIVERSITY OF NEBRASKA LINCOLN · PI ZEMPLENI, JANOS · 2006 to 2007
$396k
NIDDK NIH HHS DK063945NIDDK NIH HHS DK077816NIDDK NIH HHS R01 DK063945NIDDK NIH HHS R01 DK077816NIDDK NIH HHS R21 DK082476NIEHS NIH HHS ES015206NIEHS NIH HHS R21 ES015206
6 · The paper itself

Abstract

Holocarboxylase synthetase (HCS) catalyzes the binding of biotin to lysine (K) residues in histones H3 and H4. Histone biotinylation marks are enriched in repressed loci, including retrotransposons. Preliminary studies suggested that K16 in histone H4 is a target for biotinylation by HCS. Here we tested the hypotheses that H4K16bio is a real histone mark in human chromatin and that H4K16bio is overrepresented in repressed gene loci and repeat regions. Polyclonal rabbit anti-human H4K16bio was generated and affinity purified. An extensive series of testing with synthetic and natural targets confirmed that this new antibody is specific for H4K16bio. Using anti-H4K16bio and chromatin immunoprecipitation assays, we demonstrated that H4K16bio is overrepresented in repeat regions [pericentromeric alpha satellite repeats and long terminal repeats (LTR)] compared with euchromatin promoters. H4K16bio was also enriched in the repressed interleukin-2 gene promoter in human lymphoid cells; transcriptional activation of the interleukin-2 gene by mitogens and phorbol esters coincided with a depletion of the H4K16bio mark at the gene promoter. The enrichment of H4K16bio depended on biotin supply; the enrichment at LTR22 and promoter 1 of the sodium-dependent multivitamin transporter (SMVT) was greater in biotin-supplemented cells compared with biotin-normal and biotin-deficient cells. The enrichment of H4K16bio at LTR15 and SMVT promoter 1 was significantly lower in fibroblasts from an HCS-deficient patient compared with an HCS wild-type control. We conclude that H4K16bio is a real phenomenon and that this mark, like other biotinylation marks, is overrepresented in repressed loci where it marks HCS docking sites.

Indexed as

Repetitive Sequences, Nucleic AcidAnimalsAntibody SpecificityBiotinCarbon-Nitrogen LigasesCentromereChromatinChromatin ImmunoprecipitationEpigenetic RepressionGene Expression RegulationHistonesHolocarboxylase Synthetase DeficiencyHumansJurkat CellsLysinePromoter Regions, GeneticBiotinbiotin transporterCarbon-Nitrogen LigasesChromatinHistonesholocarboxylase synthetasesLysineSymporters

Identifiers

PMID22192339
PMCPMC3314090
OpenAlexW2159679845

What OpenQuestion holds

Textmetadata
LicenceTDM
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.