Mitochondria and calcium defects correlate with axonal dysfunction in GDAP1-related Charcot-Marie-Tooth mouse model

TRPV4 disrupts mitochondrial transport and causes axonal degeneration via a CaMKII-dependent elevation of intracellular Ca2+

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Neuroinflammation in the pathogenesis of axonal Charcot-Marie-Tooth disease caused by lack of GDAP1

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Mitochondria at the neuronal presynapse in health and disease

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CMT-linked loss-of-function mutations in GDAP1 impair store-operated Ca2+ entry-stimulated respiration

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L-Lactate-Mediated Neuroprotection against Glutamate-Induced Excitotoxicity Requires ARALAR/AGC1

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Regulation of mitochondrial transport in neurons

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Mitochondrial ATP-Mg/Pi Carrier SCaMC-3/Slc25a23 Counteracts PARP-1-Dependent Fall in Mitochondrial ATP Caused by Excitotoxic Insults in Neurons

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Mitochondrial dynamics and inherited peripheral nerve diseases

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Lack of GDAP1 Induces Neuronal Calcium and Mitochondrial Defects in a Knockout Mouse Model of Charcot-Marie-Tooth Neuropathy

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At the right distance: ER-mitochondria juxtaposition in cell life and death

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The Gdap1 knockout mouse mechanistically links redox control to Charcot–Marie–Tooth disease

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Neuronal calcium signaling: function and dysfunction

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Mitochondrial defects and neuromuscular degeneration caused by altered expression of Drosophila Gdap1: implications for the Charcot–Marie–Tooth neuropathy

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Loss of Mitochondrial Fission Depletes Axonal Mitochondria in Midbrain Dopamine Neurons

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Vesicular Glycolysis Provides On-Board Energy for Fast Axonal Transport

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Mitochondrial Cristae Shape Determines Respiratory Chain Supercomplexes Assembly and Respiratory Efficiency

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Orthogonal Functionalisation of Upconverting NaYF4Nanocrystals

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Calcium-Regulation of Mitochondrial Respiration Maintains ATP Homeostasis and Requires ARALAR/AGC1-Malate Aspartate Shuttle in Intact Cortical Neurons

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Microfluidic primary culture model of the lower motor neuron–neuromuscular junction circuit

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Mitochondria and plasma membrane Ca2+-ATPase control presynaptic Ca2+clearance in capsaicin-sensitive rat sensory neurons

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Clinical implications of genetic advances in Charcot–Marie–Tooth disease

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Silencing of the Charcot–Marie–Tooth disease-associated gene GDAP1 induces abnormal mitochondrial distribution and affects Ca2+ homeostasis by reducing store-operated Ca2+ entry

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Role of Mitochondrial Ca2+ in the Regulation of Cellular Energetics

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Mitochondrial division ensures the survival of postmitotic neurons by suppressing oxidative damage

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Decreases in plasma membrane Ca2+-ATPase in brain synaptic membrane rafts from aged rats

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Calcium signaling around Mitochondria Associated Membranes (MAMs)

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Charcot–Marie–Tooth disease CMT4A: GDAP1 increases cellular glutathione and the mitochondrial membrane potential

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Mitofusin 2 Regulates STIM1 Migration from the Ca2+Store to the Plasma Membrane in Cells with Depolarized Mitochondria

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ER Tubules Mark Sites of Mitochondrial Division

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Mitochondrial dysfunction and pathophysiology of Charcot–Marie–Tooth disease involving GDAP1 mutations

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Phenotypical features of the p.R120W mutation in the GDAP1 gene causing autosomal dominant Charcot-Marie-Tooth disease

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Alterations in bioenergetics due to changes in mitochondrial DNA copy number

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Regulation of mitochondrial dehydrogenases by calcium ions

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Endoplasmic reticulum Ca2+ release through ryanodine and IP3 receptors contributes to neuronal excitotoxicity

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The dynamin-related GTPase Drp1 is required for embryonic and brain development in mice

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KIF5B Motor Adaptor Syntabulin Maintains Synaptic Transmission in Sympathetic Neurons

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Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice

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GDAP1 mutations differ in their effects on mitochondrial dynamics and apoptosis depending on the mode of inheritance

(2009) Axel Niemann et al.   NEUROBIOLOGY OF DISEASE

Vocal cord paresis and diaphragmatic dysfunction are severe and frequent symptoms of GDAP1-associated neuropathy

(2008) T. Sevilla et al.   BRAIN

Mitofusin 2 tethers endoplasmic reticulum to mitochondria

(2008) Olga Martins de Brito et al.   NATURE

Bidirectional Ca2+-dependent control of mitochondrial dynamics by the Miro GTPase

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