RGD Reference Report - Adenylate kinase 1 gene deletion disrupts muscle energetic economy despite metabolic rearrangement. - Rat Genome Database

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

Authors: Janssen, E  Dzeja, PP  Oerlemans, F  Simonetti, AW  Heerschap, A  De Haan, A  Rush, PS  Terjung, RR  Wieringa, B  Terzic, A 
Citation: Janssen E, etal., EMBO J 2000 Dec 1;19(23):6371-81.
RGD ID: 1300280
Pubmed: PMID:11101510   (View Abstract at PubMed)
PMCID: PMC305872   (View Article at PubMed Central)
DOI: DOI:10.1093/emboj/19.23.6371   (Journal Full-text)

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.

Objects referenced in this article
Gene AK1 adenylate kinase 1 Homo sapiens
Gene Ak1 adenylate kinase 1 Mus musculus
Gene Ak1 adenylate kinase 1 Rattus norvegicus

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