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Thsi stduy Our findings bring new insight into the biology of ATP13A2 and open novel opportunities for its study using zebrafish as a model organism.
Hereditary Parkinsonism-associated genetic variations in PARK9 locus lead to functional impairment in the ion transport function of this protein. (Review)
Study unravels a novel activity-independent scaffolding role of ATP13A2 in trafficking/export of intracellular cargo in response to proteotoxic stress.
we describe, for the first time, the deleterious effect arising from the interaction between the ATP13A2 familial mutant Dup22 with a-Syn (show FYN ELISA Kits). We show that this ATP13A2 mutant can enhance a-Syn (show FYN ELISA Kits) oligomerization and aggregation in cell culture
ATP13A2 inhibition by hsa (show CD24 ELISA Kits)-miR (show MLXIP ELISA Kits)-4306 efficiently restored manganese-induced cytotoxicity in cultured neurons.
This study demonstrated that loss of ATP13A2 function causes a combination of lysosomal and mitochondrial dysfunction that affects multiple neuronal populations.
The ATP13A2 A746T variant is rare in Han Chinese patients and controls and is not associated with PD susceptibility in this ethnic group.
This study showed that LRRK2 (show LRRK2 ELISA Kits), PARK2 (show PARK2 ELISA Kits) and ATP13A2 are under copy number variations influence in patient with Parkinson disease.
tre (show TREH ELISA Kits) results of this study suggests that the expression of ATP13A2 regulated by the PHD2 (show EGLN1 ELISA Kits)-HIF1alpha (show HIF1A ELISA Kits) signaling pathway,and this is instrumental in maintaining cellular iron homeostasis and cell viability in mitochondrially compromised DAergic neurons.
that ATP13A2 contains a unique N-terminal hydrophobic extension that lies on the cytosolic membrane surface of the lysosome, where it interacts with the lysosomal signaling lipids phosphatidic acid and phosphatidylinositol(3,5)bisphosphate.
ATP13A2 overexpression improves the lysosome membrane integrity and protects against iron-induced cell damage.
the loss of Atp13a2 causes sensorimotor impairments, alpha-synuclein accumulation as occurs in PD and related synucleinopathies, and accumulation of lipofuscin deposits characteristic of NCL (show NCL ELISA Kits)
study reveals a number of intriguing neuronal phenotypes due to the loss- or gain-of-function of ATP13A2 that support a role for this protein in regulating intracellular cation homeostasis and neuronal integrity
This study showed that ATP13A2 regulates mitochondrial bioenergetics through macroautophagy.
This gene encodes a member of the P5 subfamily of ATPases which transports inorganic cations as well as other substrates. Mutations in this gene are associated with Kufor-Rakeb syndrome (KRS), also referred to as Parkinson disease 9. Multiple transcript variants encoding different isoforms have been found for this gene.
probable cation-transporting ATPase 13A2
, ATPase type 13A2
, probable cation-transporting ATPase 13A2-like
, putative ATPase