Deficiency of ATP13A2 leads to lysosomal dysfunction, α-synuclein accumulation, and neurotoxicity.

Usenovic, Marija

Deficiency of ATP13A2 leads to lysosomal dysfunction, α-synuclein accumulation, and neurotoxicity. [electronic resource] - The Journal of neuroscience : the official journal of the Society for Neuroscience Mar 2012 - 4240-6 p. digital

Publication Type: Journal Article; Research Support, N.I.H., Extramural

1529-2401

10.1523/JNEUROSCI.5575-11.2012 doi


Animals
Cells, Cultured
Cerebral Cortex--cytology
Dementia--pathology
Embryo, Mammalian
Epidermal Growth Factor--metabolism
ErbB Receptors--metabolism
Fibroblasts--metabolism
Gene Expression Regulation--genetics
Green Fluorescent Proteins--genetics
Humans
L-Lactate Dehydrogenase--metabolism
Leucine--metabolism
Lysosomal-Associated Membrane Protein 1--metabolism
Lysosomes--metabolism
Male
Mice
Mice, Inbred C57BL
Microtubule-Associated Proteins--metabolism
Mutation--genetics
Neurofilament Proteins--metabolism
Neurons--drug effects
Parkinsonian Disorders--pathology
Proton-Translocating ATPases--deficiency
RNA, Small Interfering--genetics
Statistics, Nonparametric
Time Factors
Transfection
Tritium--metabolism
alpha-Synuclein--metabolism