Evidence map›Paper›PMID 29688796›Full record

ArticleMolecular biology of the cell2018

Cardiomyopathy-associated mutation in the ADP/ATP carrier reveals translation-dependent regulation of cytochrome c oxidase activity.

Oluwaseun B Ogunbona, Matthew G Baile, Steven M Claypool

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2018. 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
1.1field-weighted citation impact, top 23% 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, 19 citations in OpenAlex.

  1. A NovelInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Life science alliance · 2019
    Article
  15. Emerging Roles in the Biogenesis of CytochromeFrontiers in cell and developmental biology · 2019
    Review
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 2 institutions in 1 country.

Oluwaseun B OgunbonaDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2185.
Matthew G BaileDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2185.
Steven M ClaypoolDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2185.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
Cardiolipin and the mitochondrial ADP/ATP carrier interactomeR01HL108882 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CLAYPOOL, STEVEN MICHAEL · 2013 to 2017
$2.0M
NHLBI NIH HHS R01 HL108882NIGMS NIH HHS T32 GM007445
6 · The paper itself

Abstract

How the absence of the major mitochondrial ADP/ATP carrier in yeast, Aac2p, results in a specific defect in cytochrome c oxidase (COX; complex IV) activity is a long-standing mystery. Aac2p physically associates with respiratory supercomplexes, which include complex IV, raising the possibility that its activity is dependent on its association with Aac2p. Here, we have leveraged a transport-dead pathogenic AAC2 point mutant to determine the basis for the reduced COX activity in the absence of Aac2p. The steady-state levels of complex IV subunits encoded by the mitochondrial genome are significantly reduced in the absence of Aac2p function, whether its association with respiratory supercomplexes is preserved or not. This diminution in COX amounts is not caused by a reduction in the mitochondrial genome copy number or the steady-state level of its transcripts, and does not reflect a defect in complex IV assembly. Instead, the absence of Aac2p activity, genetically or pharmacologically, results in an aberrant pattern of mitochondrial translation. Interestingly, compared with the complete absence of Aac2p, the complex IV-related defects are greater in mitochondria expressing the transport-inactive Aac2p mutant. Our results highlight a critical role for Aac2p transport in mitochondrial translation whose disturbance uniquely impacts cytochrome c oxidase.

Indexed as

Protein BiosynthesisCardiomyopathiesElectron Transport Complex IVGenome, MitochondrialMitochondriaMitochondrial ADP, ATP TranslocasesMutationOxidative PhosphorylationProtein StabilitySaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCOX3 protein, S cerevisiaeElectron Transport Complex IVMitochondrial ADP, ATP TranslocasesPET9 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID29688796
PMCPMC6014099
OpenAlexW2801380699

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.