Evidence map›Paper›PMID 20544879›Full record

ReviewEnvironmental and molecular mutagenesis2010

A compendium of human mitochondrial gene expression machinery with links to disease.

Timothy E Shutt, Gerald S Shadel

Open access · bronzeAbstract readReview
In one paragraph

Review in Environmental and molecular mutagenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Mitochondrial Proteostasis Requires Genes Encoded in a Neurodevelopmental Syndrome Locus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. AMPK: implications in osteoarthritis and therapeutic targets.American journal of translational research · 2020
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Role of microRNA in metabolic shift during heart failure.American journal of physiology. Heart and circulatory physiology · 2017
    Review
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Timothy E ShuttDepartment of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA.
Gerald S Shadel
Yale University · US

Funding

Nuclear Control of Mitochondrial Gene ExpressionR01HL059655 · NHLBI · YALE UNIVERSITY · PI SHADEL, GERALD · 1997 to 2011
$3.1M
Mitochondrial Dysfunction and Oxidative Stress in Ataxia TelangiectasiaR01NS056206 · NINDS · YALE UNIVERSITY · PI SHADEL, GERALD · 2007 to 2011
$1.9M
NHLBI NIH HHS HL-059655NHLBI NIH HHS R01 HL059655NINDS NIH HHS R01 NS056206
6 · The paper itself

Abstract

Mammalian mitochondrial DNA encodes 37 essential genes required for ATP production via oxidative phosphorylation, instability or misregulation of which is associated with human diseases and aging. Other than the mtDNA-encoded RNA species (13 mRNAs, 12S and 16S rRNAs, and 22 tRNAs), the remaining factors needed for mitochondrial gene expression (i.e., transcription, RNA processing/modification, and translation), including a dedicated set of mitochondrial ribosomal proteins, are products of nuclear genes that are imported into the mitochondrial matrix. Herein, we inventory the human mitochondrial gene expression machinery, and, while doing so, we highlight specific associations of these regulatory factors with human disease. Major new breakthroughs have been made recently in this burgeoning area that set the stage for exciting future studies on the key outstanding issue of how mitochondrial gene expression is regulated differentially in vivo. This should promote a greater understanding of why mtDNA mutations and dysfunction cause the complex and tissue-specific pathology characteristic of mitochondrial disease states and how mitochondrial dysfunction contributes to more common human pathology and aging.

Indexed as

Genes, MitochondrialAdenosine TriphosphateDiseaseDNA, MitochondrialGene ExpressionHumansMitochondriaMitochondrial DiseasesMitochondrial ProteinsRibosomesRNARNA, MitochondrialTranscription, GeneticAdenosine TriphosphateDNA, MitochondrialMitochondrial ProteinsRNARNA, Mitochondrial

Identifiers

PMID20544879
PMCPMC2886302
OpenAlexW2155648855

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.