Evidence map›Paper›PMID 26635618›Full record

ArticleFrontiers in physiology2015

Protein Kinase A Governs Oxidative Phosphorylation Kinetics and Oxidant Emitting Potential at Complex I.

Daniel S Lark, Lauren R Reese, Terence E Ryan, Maria J Torres, Cody D Smith, Chien-Te Lin, P Darrell Neufer

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2015. 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
0.9field-weighted citation impact, top 25% 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, 26 citations in OpenAlex.

  1. Review
  2. The role of soluble adenylyl cyclase in sensing and regulating intracellular pH.Pflugers Archiv : European journal of physiology · 2024
    Review
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  12. Mitochondrial respiration and HAmerican journal of physiology. Cell physiology · 2019
    Article
  13. Article
  14. Melatonin and the electron transport chain.Cellular and molecular life sciences : CMLS · 2017
    Review
  15. 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

7 authors at 1 institution in 1 country.

Daniel S LarkEast Carolina Diabetes and Obesity Institute Greenville, NC, USA ; Department of Kinesiology, East Carolina University Greenville, NC, USA.
Lauren R ReeseEast Carolina Diabetes and Obesity Institute Greenville, NC, USA ; Department of Physiology, Brody School of Medicine, East Carolina University Greenville, NC, USA.
Terence E RyanEast Carolina Diabetes and Obesity Institute Greenville, NC, USA ; Department of Physiology, Brody School of Medicine, East Carolina University Greenville, NC, USA.
Maria J TorresEast Carolina Diabetes and Obesity Institute Greenville, NC, USA ; Department of Kinesiology, East Carolina University Greenville, NC, USA.
Cody D SmithEast Carolina Diabetes and Obesity Institute Greenville, NC, USA ; Department of Physiology, Brody School of Medicine, East Carolina University Greenville, NC, USA.
Chien-Te LinEast Carolina Diabetes and Obesity Institute Greenville, NC, USA ; Department of Physiology, Brody School of Medicine, East Carolina University Greenville, NC, USA.
P Darrell NeuferEast Carolina Diabetes and Obesity Institute Greenville, NC, USA ; Department of Kinesiology, East Carolina University Greenville, NC, USA ; Department of Physiology, Brody School of Medicine, East Carolina University Greenville, NC, USA.
East Carolina University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitochondrial electron transport system (ETS) is responsible for setting and maintaining both the energy and redox charges throughout the cell. Reversible phosphorylation of mitochondrial proteins, particularly via the soluble adenylyl cyclase (sAC)/cyclic AMP (cAMP)/Protein kinase A (PKA) axis, has recently been revealed as a potential mechanism regulating the ETS. However, the governance of cAMP/PKA signaling and its implications on ETS function are incompletely understood. In contrast to prior reports using exogenous bicarbonate, we provide evidence that endogenous CO2 produced by increased tricarboxylic acid (TCA) cycle flux is insufficient to increase mitochondrial cAMP levels, and that exogenous addition of membrane permeant 8Br-cAMP does not enhance mitochondrial respiratory capacity. We also report important non-specific effects of commonly used inhibitors of sAC which preclude their use in studies of mitochondrial function. In isolated liver mitochondria, inhibition of PKA reduced complex I-, but not complex II-supported respiratory capacity. In permeabilized myofibers, inhibition of PKA lowered both the K m and V max for complex I-supported respiration as well as succinate-supported H2O2 emitting potential. In summary, the data provided here improve our understanding of how mitochondrial cAMP production is regulated, illustrate a need for better tools to examine the impact of sAC activity on mitochondrial biology, and suggest that cAMP/PKA signaling contributes to the governance of electron flow through complex I of the ETS.

Indexed as

adenylyl cyclasecAMPcomplex Ilivermitochondriaprotein kinase Arespirationskeletal muscle

Identifiers

PMID26635618
PMCPMC4646981
OpenAlexW2191385375

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.