Disruption in the autophagic process underlies the sensory neuropathy in dystonia musculorum mice

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Transgenic expression of neuronal dystonin isoform 2 partially rescues the disease phenotype of the dystonia musculorum mouse model of hereditary sensory autonomic neuropathy VI

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dnc-1/dynactin 1 Knockdown Disrupts Transport of Autophagosomes and Induces Motor Neuron Degeneration

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Hereditary sensory autonomic neuropathy caused by a mutation in dystonin

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Autophagosomes initiate distally and mature during transport toward the cell soma in primary neurons

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Microtubule stability, Golgi organization, and transport flux require dystonin-a2–MAP1B interaction

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Selective autophagy mediated by autophagic adapter proteins

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Mitochondria removal by autophagy

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MAP1B and Clathrin Are Novel Interacting Partners of the Giant Cyto-linker Dystonin

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Neuronal dystonin isoform 2 is a mediator of endoplasmic reticulum structure and function

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Acetylated microtubules are required for fusion of autophagosomes with lysosomes

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Starvation-induced Hyperacetylation of Tubulin Is Required for the Stimulation of Autophagy by Nutrient Deprivation

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Autophagy gone awry in neurodegenerative diseases

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Multiple roles of the cytoskeleton in autophagy

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Dynein light chain 1 is required for autophagy, protein clearance, and cell death in Drosophila

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Dynein-dependent Movement of Autophagosomes Mediates Efficient Encounters with Lysosomes

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Dystonin/Bpag1 is a necessary endoplasmic reticulum/nuclear envelope protein in sensory neurons

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The Itinerary of Autophagosomes: From Peripheral Formation to Kiss-and-Run Fusion with Lysosomes

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