Haploinsufficiency of AFG3L2, the gene responsible for spinocerebellar ataxia type 28, causes mitochondria-mediated Purkinje cell dark degeneration. (Q45922719)

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scientific article published in July 2009

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English	Haploinsufficiency of AFG3L2, the gene responsible for spinocerebellar ataxia type 28, causes mitochondria-mediated Purkinje cell dark degeneration.	scientific article published in July 2009

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scholarly article

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3 February 2020

Haploinsufficiency of AFG3L2, the gene responsible for spinocerebellar ataxia type 28, causes mitochondria-mediated Purkinje cell dark degeneration (English)

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haploinsufficiency

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spinocerebellar ataxia type 28

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Angelo Quattrini

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author name string

Francesca Maltecca

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Raffaella Magnoni

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Federica Cerri

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Gregory A Cox

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1 July 2009

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Journal of Neuroscience

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29

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9244-9254

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3 February 2020

Characterization of progressive motor deficits in mice transgenic for the human Huntington's disease mutation.

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Chaperone-like activity of the AAA domain of the yeast Yme1 AAA protease

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Glutamate-induced neuron death requires mitochondrial calcium uptake

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Behavioral phenotyping of transgenic and knockout mice: experimental design and evaluation of general health, sensory functions, motor abilities, and specific behavioral tests

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Epitope-tagged P(0) glycoprotein causes Charcot-Marie-Tooth-like neuropathy in transgenic mice.

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Hypoxia induces an excitotoxic-type of dark cell degeneration in cerebellar Purkinje neurons

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Polyglutamine-expanded ataxin-7 promotes non-cell-autonomous purkinje cell degeneration and displays proteolytic cleavage in ataxic transgenic mice.

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The molecular organization of cerebellar long-term depression

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Spatial learning, exploration, anxiety, and motor coordination in female APP23 transgenic mice with the Swedish mutation

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Interactions between mitochondrial bioenergetics and cytoplasmic calcium in cultured cerebellar granule cells.

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A note on a simple apparatus for detecting neurological deficit in rats and mice

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Patterned Purkinje cell death in the cerebellum

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Loss of m-AAA protease in mitochondria causes complex I deficiency and increased sensitivity to oxidative stress in hereditary spastic paraplegia

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AMPA-induced dark cell degeneration of cerebellar Purkinje neurons involves activation of caspases and apparent mitochondrial dysfunction

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Recent advances in the analysis of oxidized proteins

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Transgenic mice expressing F3/contactin from the transient axonal glycoprotein promoter undergo developmentally regulated deficits of the cerebellar function.

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Axonal degeneration in paraplegin-deficient mice is associated with abnormal mitochondria and impairment of axonal transport

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Cellular and genetic regulation of the development of the cerebellar system

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Cerebellar ataxia and Purkinje cell dysfunction caused by Ca2+-activated K+ channel deficiency

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Calcium, ATP, and ROS: a mitochondrial love-hate triangle

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Role of oxidative carbonylation in protein quality control and senescence

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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

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The m-AAA protease defective in hereditary spastic paraplegia controls ribosome assembly in mitochondria

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SCA28, a novel form of autosomal dominant cerebellar ataxia on chromosome 18p11.22-q11.2.

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The role of mitochondria in inherited neurodegenerative diseases

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Mitochondrial disease

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Mitochondria: more than just a powerhouse

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Bergmann glia expression of polyglutamine-expanded ataxin-7 produces neurodegeneration by impairing glutamate transport.

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Targeted deletion of a single Sca8 ataxia locus allele in mice causes abnormal gait, progressive loss of motor coordination, and Purkinje cell dendritic deficits

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Variable and tissue-specific subunit composition of mitochondrial m-AAA protease complexes linked to hereditary spastic paraplegia

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Mitochondrial trafficking and morphology in healthy and injured neurons

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Protein degradation within mitochondria: versatile activities of AAA proteases and other peptidases

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Cytoskeletal protein carbonylation and degradation in experimental autoimmune encephalomyelitis

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The mitochondrial protease AFG3L2 is essential for axonal development

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Mitochondria in neuroplasticity and neurological disorders

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Genetic interaction between the m-AAA protease isoenzymes reveals novel roles in cerebellar degeneration

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Determination of carbonyl content in oxidatively modified proteins

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One trial learning in the mouse. I. Its characteristics and modification by experimental-seasonal variables

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Analysis of molecular masses and oligomeric states of protein complexes by blue native electrophoresis and isolation of membrane protein complexes by two-dimensional native electrophoresis

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12 December 2020

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https://pubmed.ncbi.nlm.nih.gov/19625515

12 December 2020

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Beta 4 integrin and other Schwann cell markers in axonal neuropathy

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12 December 2020

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Use of fibroblast and lymphoblast cultures for detection of respiratory chain defects

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Behavioral and functional analysis of mouse phenotype: SHIRPA, a proposed protocol for comprehensive phenotype assessment

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Identifiers

10.1523/JNEUROSCI.1532-09.2009

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3 February 2020

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3 February 2020

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