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Key Documents

A9732

Sigma-Aldrich

Anti-ATP13A2 (C-terminal) antibody produced in rabbit

enhanced validation

~1.5 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonyme(s) :

Anti-ATPase type 13A2, Anti-PARK9

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~129 kDa

Espèces réactives

mouse, human

Validation améliorée

recombinant expression
Learn more about Antibody Enhanced Validation

Concentration

~1.5 mg/mL

Technique(s)

western blot: 1-2 μg/mL using mouse brain extract (S1 fraction)
western blot: 2-4 μg/mL using extract of HEK-293T cells expressing human ATP13A2

Numéro d'accès UniProt

Q9NQ11

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ATP13A2(23400)
mouse ... Atp13a2(74772)

Catégories apparentées

Description générale

ATP13A2 is a member of the P5 family of ATPases which function in the transport of inorganic cations.
ATPase type 13 A2 (ATP13A2), also known as Parkinson′s disease 9 (PARK9), codes for P-type ATPase that is present on the lysosomal membrane with ten transmembrane domains.

Application

Anti-ATP13A2 (C-terminal) antibody produced in rabbit has also been used in immunohistochemistry.
Rabbit Anti-ATP13A2 (C-terminal) antibody has be used for immunofluorescence and western blotting assays.

Actions biochimiques/physiologiques

ATPase type 13A2 (ATP13A2) plays a vital role in regulation of mitochondrial bioenergetics by macroautophagy. Mutations in the ATP13A2 gene leads to the development of hereditary form of Parkinson associated with dementia, known as Kufor-Rakeb syndrome (KRS).

Forme physique

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

10 - Combustible liquids

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Karen E Murphy et al.
Acta neuropathologica communications, 1, 11-11 (2013-11-21)
ATP13A2 (PARK9) loss of function mutations are a genetic cause of an early-onset form of Parkinson's disease (PD), with in vitro studies showing that ATP13A2 deficits lead to lysosomal and mitochondrial dysfunction and α-synuclein accumulation, while elevated ATP13A2 expression reduces
Aaron M Gusdon et al.
Neurobiology of disease, 45(3), 962-972 (2011-12-27)
Mitochondrial dysfunction and autophagy are centrally implicated in Parkinson's disease (PD). Mutations in ATP13A2, which encodes a lysosomal P-type ATPase of unknown function, cause a rare, autosomal recessive parkinsonian syndrome. Lysosomes are essential for autophagy, and autophagic clearance of dysfunctional
David Ramonet et al.
Human molecular genetics, 21(8), 1725-1743 (2011-12-22)
Mutations in the ATP13A2 gene (PARK9, OMIM 610513) cause autosomal recessive, juvenile-onset Kufor-Rakeb syndrome and early-onset parkinsonism. ATP13A2 is an uncharacterized protein belonging to the P(5)-type ATPase subfamily that is predicted to regulate the membrane transport of cations. The physiological
Jason P Covy et al.
Journal of neuroscience research, 90(12), 2306-2316 (2012-08-01)
Mutations in ATP13A2, which encodes a lysosomal P-type ATPase of unknown function, cause an autosomal recessive parkinsonian syndrome. With mammalian cells, we show that ATP13A2 expression protects against manganese and nickel toxicity, in addition to proteasomal, mitochondrial, and oxidative stress.

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