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anti-Mouse (Murine) ATP13A2 Antikörper:
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Human Polyclonal ATP13A2 Primary Antibody für IHC, SimWes - ABIN188923
Henry, Aghamohammadzadeh, Samaroo, Chen, Mou, Needle, Hirst: Pathogenic LRRK2 mutations, through increased kinase activity, produce enlarged lysosomes with reduced degradative capacity and increase ATP13A2 expression. in Human molecular genetics 2015
Show all 2 Pubmed References
Polyclonal ATP13A2 Primary Antibody für IHC (fro), WB - ABIN540775
Ramirez, Heimbach, Gründemann, Stiller, Hampshire, Cid, Goebel, Mubaidin, Wriekat, Roeper, Al-Din, Hillmer, Karsak, Liss, Woods, Behrens, Kubisch: Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase. in Nature genetics 2006
Study shows for the first time in vivo that loss of function of ATP13A2 causes an increased sensitivity to manganese.
Loss of one functional Atp13a2 allele leads to selective gliosis independent of robust lipofuscinosis.
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
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.
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.
ATP13A2 and SYT11 form a functional network in the regulation of the autophagy-lysosome pathway, which may contribute to forms of Parkinson's Disease-associated neurodegeneration.
This study showed that Lysosomal defects in ATP13A2 associated familial Parkinson's disease.
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. We show that this ATP13A2 mutant can enhance a-Syn oligomerization and aggregation in cell culture
ATP13A2 inhibition by hsa-miR-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, PARK2 and ATP13A2 are under copy number variations influence in patient with Parkinson disease.
tre results of this study suggests that the expression of ATP13A2 regulated by the PHD2-HIF1alpha 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.
these data suggest the involvement of PARK9 in the biogenesis of exosomes and alpha-synuclein secretion.
Reduced ATP13A2 expression significantly decreased vesicular zinc levels, indicating ATP13A2 facilitates transport of zinc.
human ATP13A2 deficiency results in zinc dyshomeostasis and mitochondrial dysfunction.
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.
ATPase type 13A2
, probable cation-transporting ATPase 13A2
, putative ATPase
, probable cation-transporting ATPase 13A2-like