Evidence map›Paper›PMID 20357078›Full record

ArticleThe Journal of nutrition2010

Biotin requirements are lower in human Jurkat lymphoid cells but homeostatic mechanisms are similar to those of HepG2 liver cells.

Gaganpreet Kaur Mall, Yap Ching Chew, Janos Zempleni

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutrition, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Changes in the Immunity, Histopathology, and Metabolism of Crayfish (Animals : an open access journal from MDPI · 2022
    Article
  3. Article
  4. Article
  5. Biotin rescues mitochondrial dysfunction and neurotoxicity in a tauopathy model.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  6. Article
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  9. Review
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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.

Gaganpreet Kaur MallDepartment of Nutrition and Health Sciences, University of Nebraska, Lincoln, NE 68583, USA.
Yap Ching Chew
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 DK082476NIEHS NIH HHS ES015206
6 · The paper itself

Abstract

The following proteins are candidates for maintaining biotin homeostasis in humans: the biotin transporters sodium-dependent multivitamin transporter (SMVT) and monocarboxylate transporter 1, the biotinyl-protein ligase holocarboxylase synthetase (HCS), and the lysine-epsilon-biotin hydrolase biotinidase. Liver cells are supplied through the portal vein with high levels of water-soluble vitamins compared with those of peripheral tissues. We hypothesized that the mechanisms of biotin homeostasis are qualitatively and quantitatively different in cells derived from human liver (HepG2 cells) and lymphoid tissues (Jurkat cells). Cells were cultured in biotin-defined media, representing deficient (D), normal (N), and supplemented (S) individuals. Biotinylation of carboxylases depended on biotin availability in both cell types, but HepG2 cells required 3 times more biotin than Jurkat cells to maintain normal levels of holocarboxylases. The expression of biotin transporters was less in both types in medium S compared with cells in media D and N; in contrast, the expression of HCS was higher in cells in medium S compared with the other cells. The abundance of 3-methylcrotonyl-CoA carboxylase mRNA was lower in cells in medium D than cells in media N and S. The enrichment of biotinylated histones was higher at the SMVT promoter 1 in HepG2 and Jurkat cells in medium S compared with the corresponding cells in media D and N, presumably repressing the SMVT gene. The mechanisms of biotin homeostasis are qualitatively similar but quantitatively different in HepG2 and Jurkat cells; HCS, histone biotinylation, and biotin transporters play a role in homeostasis in both.

Indexed as

BiotinBiotinylationCarboxy-LyasesCulture MediaHepatocytesHep G2 CellsHistonesHomeostasisHumansJurkat CellsLymphocytesBiotinCarboxy-LyasesCulture MediaHistones

Identifiers

PMID20357078
PMCPMC2869498
OpenAlexW2164451611

What OpenQuestion holds

Textmetadata
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.