ArticleBMC neuroscience2008
Creatine kinase B deficient neurons exhibit an increased fraction of motile mitochondria.
Article in BMC neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- The effect of the creatine analogue beta-guanidinopropionic acid on energy metabolism: a systematic review.PloS one · 2013Pooled it
- Current Methods of Magnetic Resonance for Noninvasive Assessment of Molecular Aspects of Pathoetiology in Multiple Sclerosis.International journal of molecular sciences · 2020Review
- The bioenergetics of neuronal morphogenesis and regeneration: Frontiers beyond the mitochondrion.Developmental neurobiology · 2020Review
- Chronic dietary creatine enhances hippocampal-dependent spatial memory, bioenergetics, and levels of plasticity-related proteins associated with NF-κB.Learning & memory (Cold Spring Harbor, N.Y.) · 2018Article
- Postsynaptic Proteome of Non-Demented Individuals with Alzheimer's Disease Neuropathology.Journal of Alzheimer's disease : JAD · 2018Article
- Creatine transporter deficiency leads to increased whole body and cellular metabolism.Amino acids · 2016Article
- The role of mitochondrially derived ATP in synaptic vesicle recycling.The Journal of biological chemistry · 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
- Astrocyte-neuron lactate shuttle may boost more ATP supply to the neuron under hypoxic conditions--in silico study supported by in vitro expression data.BMC systems biology · 2011Article
- 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
- Synaptic mitochondria in synaptic transmission and organization of vesicle pools in health and disease.Frontiers in synaptic neuroscience · 2010Article
- HUMMR, a hypoxia- and HIF-1alpha-inducible protein, alters mitochondrial distribution and transport.The Journal of cell biology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeurons require an elaborate system of intracellular transport to distribute cargo throughout axonal and dendritic projections. Active anterograde and retrograde transport of mitochondria serves in local energy distribution, but at the same time also requires input of ATP. Here we studied whether brain-type creatine kinase (CK-B), a key enzyme for high-energy phosphoryl transfer between ATP and CrP in brain, has an intermediary role in the reciprocal coordination between mitochondrial motility and energy distribution. Therefore, we analysed the impact of brain-type creatine kinase (CK-B) deficiency on transport activity and velocity of mitochondria in primary murine neurons and made a comparison to the fate of amyloid precursor protein (APP) cargo in these cells, using live cell imaging.
resultsComparison of average and maximum transport velocities and global transport activity showed that CK-B deficiency had no effect on speed of movement of mitochondria or APP cargo, but that the fraction of motile mitochondria was significantly increased by 36% in neurons derived from CK-B knockout mice. The percentage of motile APP vesicles was not altered.
conclusionCK-B activity does not directly couple to motor protein activity but cells without the enzyme increase the number of motile mitochondria, possibly as an adaptational strategy aimed to enhance mitochondrial distribution versatility in order to compensate for loss of efficiency in the cellular network for ATP distribution.
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