Evidence map›Paper›PMID 20618965›Full record

ArticleBMC biochemistry2010

Loss of the SIN3 transcriptional corepressor results in aberrant mitochondrial function.

Valerie L Barnes, Bethany S Strunk, Icksoo Lee, Maik Hüttemann, Lori A Pile

Open access · hybridAbstract read
In one paragraph

Article in BMC biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

15 citing papers in PubMed, 31 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

5 authors at 2 institutions in 1 country.

Valerie L BarnesDepartment of Biological Sciences, Wayne State University, Detroit, Michigan 48202, USA.
Bethany S Strunk
Icksoo Lee
Maik Hüttemann
Lori A Pile
Wayne State University · USUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSIN3 is a transcriptional repressor protein known to regulate many genes, including a number of those that encode mitochondrial components.

resultsBy monitoring RNA levels, we find that loss of SIN3 in Drosophila cultured cells results in up-regulation of not only nuclear encoded mitochondrial genes, but also those encoded by the mitochondrial genome. The up-regulation of gene expression is accompanied by a perturbation in ATP levels in SIN3-deficient cells, suggesting that the changes in mitochondrial gene expression result in altered mitochondrial activity. In support of the hypothesis that SIN3 is necessary for normal mitochondrial function, yeast sin3 null mutants exhibit very poor growth on non-fermentable carbon sources and show lower levels of ATP and reduced respiration rates.

conclusionsThe findings that both yeast and Drosophila SIN3 affect mitochondrial activity suggest an evolutionarily conserved role for SIN3 in the control of cellular energy production.

Indexed as

Adenosine TriphosphateAnimalsCells, CulturedDrosophilaDrosophila ProteinsGene Knockdown TechniquesMitochondriaRespiratory RateRNA InterferenceSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSin3 Histone Deacetylase and Corepressor ComplexAdenosine TriphosphateDrosophila ProteinsSaccharomyces cerevisiae ProteinsSin3 Histone Deacetylase and Corepressor Complex

Identifiers

PMID20618965
PMCPMC2909972
OpenAlexW2025022105

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.