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ATP13A2 encodes a member of the P5 subfamily of ATPases which transports inorganic cations as well as other substrates. Additionally we are shipping ATP13A2 Antibodies (63) and ATP13A2 Proteins (9) and many more products for this protein.
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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.
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.
A review of recent advances in the emerging association of ATP13A2 mutations with Parkinsonism and neuronal ceroid lipofuscinoses.
The mutation rates of Thr12Met and Ala1144Thr of ATP13A2 in the Uygur and Han Parkinson's disease patients in the Xinjiang region are low.
This study demonistrated that loss of ATP13A2 causes a specific protein trafficking defect, and that Atp13a2 null mice develop age-related motor dysfunction that is preceded by neuropathological changes.
Data show that patients with Lewy body diseases have an overall deficit in ATP13A2 protein levels, with the remaining protein being more insoluble and partially redistributing towards Lewy bodies
Present results of homozygosity mapping in two siblings affected with early onset Parkinson's disease (EOPD) and mutation screening of ATP13A2. The variation identified represents the 13th known disease causing mutation in ATP13A2.
the loss of Atp13a2 causes sensorimotor impairments, alpha-synuclein (show SNCA ELISA Kits) 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