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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

Sinónimos:

Anti-ATPase type 13A2, Anti-PARK9

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~129 kDa

species reactivity

mouse, human

enhanced validation

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

UniProt accession no.

Q9NQ11

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

Categorías relacionadas

General description

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.

Biochem/physiol Actions

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).

Physical form

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

Disclaimer

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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Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

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

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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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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