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Key Documents

A9607

Sigma-Aldrich

Anti-ATP13A2 antibody produced in rabbit

enhanced validation

~1 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 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

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)
rat ... Atp13a2(362645)

Description générale

ATP13A2 is a member of the P5 family of ATPases which function in the transport of inorganic cations.
ATPase type 13A2 (ATP13A2) is a neuronal P-type ATPAse. The gene is also referref as PARK9 (Parkinson′s disease 9).
Rabbit Anti-ATP13A2 antibody binds to human and mouse ATP13A2.

Application

Rabbit Anti-ATP13A2 antibody has been used for western blot assays.

Actions biochimiques/physiologiques

Mutations in the gene encoding ATPase type 13A2 (ATP13A2) is implicated with a hereditary form of PD associated with dementia, known as Kufor-Rakeb syndrome (KRS). ATP13A2 shows elevated expression levels in brains of sporadic PD patients, suggesting a potential role in the more common forms of Parkinson′s disease.

Forme physique

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

Autres remarques

2024 CiteAb Award Winner for Supplier Succeeding in Parkinson′s Research

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

Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase
Ramirez A, et al.
Nature Genetics, 38(10), 1184-1184 (2006)
Patrick J Schultheis et al.
Human molecular genetics, 22(10), 2067-2082 (2013-02-09)
Mutations in ATP13A2 (PARK9), encoding a lysosomal P-type ATPase, are associated with both Kufor-Rakeb syndrome (KRS) and neuronal ceroid lipofuscinosis (NCL). KRS has recently been classified as a rare genetic form of Parkinson's disease (PD), whereas NCL is a lysosomal
Yuta Hatori et al.
PloS one, 17(11), e0276823-e0276823 (2022-11-30)
Mutations in ATP13A2 cause Kufor-Rakeb Syndrome (KRS), a juvenile form of Parkinson's Disease (PD). The gene product belongs to a diverse family of ion pumps and mediates polyamine influx from lysosomal lumen. While the biochemical and structural studies highlight its
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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