ArticleMolecular and cellular biochemistry1998
Cytoarchitectural and metabolic adaptations in muscles with mitochondrial and cytosolic creatine kinase deficiencies.
Article in Molecular and cellular biochemistry, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 88 citations in OpenAlex.
- Optimal neuromuscular performance requires motor neuron phosphagen kinases.The Journal of physiology · 2026Article
- Genetic Determinants of Creatine Bioavailability and Responsiveness: Emphasis on Common Low-Impact Variants.Lifestyle genomics · 2026Review
- A covalent creatine kinase inhibitor ablates glioblastoma migration and sensitizes tumors to oxidative stress.Scientific reports · 2024Article
- Depletion of creatine phosphagen energetics with a covalent creatine kinase inhibitor.Nature chemical biology · 2023Article
- Ontogeny of cardiomyocytes: ultrastructure optimization to meet the demand for tight communication in excitation-contraction coupling and energy transfer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Energy metabolism design of the striated muscle cell.Physiological reviews · 2021Review
- Creatine metabolism: energy homeostasis, immunity and cancer biology.Nature reviews. Endocrinology · 2020Review
- A Mouse Model of Creatine Transporter Deficiency Reveals Impaired Motor Function and Muscle Energy Metabolism.Frontiers in physiology · 2018Article
- Nutrition and Training Influences on the Regulation of Mitochondrial Adenosine Diphosphate Sensitivity and Bioenergetics.Sports medicine (Auckland, N.Z.) · 2017Review
- The extended, dynamic mitochondrial reticulum in skeletal muscle and the creatine kinase (CK)/phosphocreatine (PCr) shuttle are working hand in hand for optimal energy provision.Journal of muscle research and cell motility · 2015Article
- Synergistic action of dendritic mitochondria and creatine kinase maintains ATP homeostasis and actin dynamics in growing neuronal dendrites.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- CKMT1 regulates the mitochondrial permeability transition pore in a process that provides evidence for alternative forms of the complex.Journal of cell science · 2014Article
- Disturbed energy metabolism and muscular dystrophy caused by pure creatine deficiency are reversible by creatine intake.The Journal of physiology · 2013Article
- Metabolomic and Lipidomic Analysis of the Heart of Peroxisome Proliferator-Activated Receptor-γ Coactivator 1-β Knock Out Mice on a High Fat Diet.Metabolites · 2012Article
- Similar mitochondrial activation kinetics in wild-type and creatine kinase-deficient fast-twitch muscle indicate significant Pi control of respiration.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- The creatine kinase system and pleiotropic effects of creatine.Amino acids · 2011Review
- Flow of energy in the outer retina in darkness and in light.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Phosphocreatine as an energy source for actin cytoskeletal rearrangements during myoblast fusion.The Journal of physiology · 2008Article
- Inhibition of cytosolic and mitochondrial creatine kinase by siRNA in HaCaT- and HeLaS3-cells affects cell viability and mitochondrial morphology.Molecular and cellular biochemistry · 2007Article
- Increased resistance to fatigue in creatine kinase deficient muscle is not due to improved contractile economy.Pflugers Archiv : European journal of physiology · 2006Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have blocked creatine kinase (CK) mediated phosphocreatine (PCr) <==> ATP transphosphorylation in mitochondria and cytosol of skeletal muscle by knocking out the genes for the mitochondrial (ScCKmit) and the cytosolic (M-CK) CK isoforms in mice. Animals which carry single or double mutations, if kept and tested under standard laboratory conditions, have surprisingly mild changes in muscle physiology. Strenuous ex vivo conditions were necessary to reveal that MM-CK absence in single and double mutants leads to a partial loss of tetanic force output. Single ScCKmit deficiency has no noticeable effects but in combination the mutations cause slowing of the relaxation rate. Importantly, our studies revealed that there is metabolic and cytoarchitectural adaptation to CK defects in energy metabolism. The effects involve mutation type-dependent alterations in the levels of AMP, IMP, glycogen and phosphomonoesters, changes in activity of metabolic enzymes like AMP-deaminase, alterations in mitochondrial volume and contractile protein (MHC isoform) profiles, and a hyperproliferation of the terminal cysternae of the SR (in tubular aggregates). This suggests that there is a compensatory resiliency of loss-of-function and redirection of flux distributions in the metabolic network for cellular energy in our mutants.
Indexed as
Identifiers
9746321W2167120395What OpenQuestion holds
Registered trials
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.