Evidence map›Paper›PMID 11101510›Full record

ArticleThe EMBO journal2000

Adenylate kinase 1 gene deletion disrupts muscle energetic economy despite metabolic rearrangement.

E Janssen, P P Dzeja, F Oerlemans, A W Simonetti, A Heerschap, A de Haan, P S Rush, R R Terjung, B Wieringa, A Terzic

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

54 citing papers in PubMed, 153 citations in OpenAlex.

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  12. Adenylate kinase AK2 isoform integral in embryo and adult heart homeostasis.Biochemical and biophysical research communications · 2021
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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

10 authors at 1 institution in 1 country.

E JanssenDepartments of Cell Biology and Diagnostic Radiology, University Medical Center, University of Nijmegen, Institute for Fundamental and Clinical Human Movement Sciences, Vrije University Amsterdam, The Netherlands.
P P Dzeja
F Oerlemans
A W Simonetti
A Heerschap
A de Haan
P S Rush
R R Terjung
B Wieringa
A Terzic
Radboud University Medical Center · NL

Funding

CARDIOVASOLOGYT32HL007111 · NHLBI · MAYO CLINIC ROCHESTER · PI Barry A. Borlaug · 1985 to 2026
$8.7M
COUPLING OF K ATP CHANNELS WITH CARDIAC ENERGETICSR01HL064822 · NHLBI · MAYO CLINIC ROCHESTER · PI TERZIC, ANDRE · 2000 to 2007
$2.4M
ADENINE NUCLEOTIDE METABOLISM IN SKELETAL MUSCLER01AR021617 · NIAMS · UPSTATE MEDICAL UNIVERSITY · PI TERJUNG, RONALD L · 1986 to 2004
$1.7M
ADENINE NUCLEOTIDE METABOLISM IN SKELETAL MUSCLER37AR021617 · NIAMS · UPSTATE MEDICAL UNIVERSITY · PI TERJUNG, RONALD L · 1989 to 1998
–
NHLBI NIH HHS HL07111NHLBI NIH HHS HL64822NHLBI NIH HHS R01 HL064822NHLBI NIH HHS T32 HL007111NIAMS NIH HHS AR21617NIAMS NIH HHS R01 AR021617NIAMS NIH HHS R37 AR021617
6 · The paper itself

Abstract

Efficient cellular energy homeostasis is a critical determinant of muscle performance, providing evolutionary advantages responsible for species survival. Phosphotransfer reactions, which couple ATP production and utilization, are thought to play a central role in this process. Here, we provide evidence that genetic disruption of AK1-catalyzed ss-phosphoryl transfer in mice decreases the potential of myofibers to sustain nucleotide ratios despite up-regulation of high-energy phosphoryl flux through glycolytic, guanylate and creatine kinase phosphotransfer pathways. A maintained contractile performance of AK1-deficient muscles was associated with higher ATP turnover rate and larger amounts of ATP consumed per contraction. Metabolic stress further aggravated the energetic cost in AK1(-/-) muscles. Thus, AK1-catalyzed phosphotransfer is essential in the maintenance of cellular energetic economy, enabling skeletal muscle to perform at the lowest metabolic cost.

Indexed as

Gene DeletionAdenineAdenosine TriphosphateAdenylate KinaseAnimalsBlotting, NorthernCatalysisCloning, MolecularCreatine KinaseEmbryo, MammalianGlucose-6-PhosphateGuanosine DiphosphateGuanosine TriphosphateGuanylate KinasesHydrogen-Ion ConcentrationHypoxiaAdenineAdenosine TriphosphateAdenylate Kinaseadenylate kinase 1Creatine KinaseGlucose-6-PhosphateGuanosine DiphosphateGuanosine TriphosphateGuanylate KinasesIsoenzymesNucleoside-Phosphate KinasePhosphotransferasesPotassium ChlorideProtein Isoforms

Identifiers

PMID11101510
PMCPMC305872
OpenAlexW2068884058

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.