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A9732

Sigma-Aldrich

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

enhanced validation

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

Synonym(e):

Anti-ATPase type 13A2, Anti-PARK9

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About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

rabbit

Qualitätsniveau

200

Konjugat

unconjugated

Antikörperform

affinity isolated antibody

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Form

buffered aqueous solution

Mol-Gew.

antigen ~129 kDa

Speziesreaktivität

mouse, human

Erweiterte Validierung

recombinant expression
Learn more about Antibody Enhanced Validation

Konzentration

~1.5 mg/mL

Methode(n)

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-Hinterlegungsnummer

Q9NQ11

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

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

Verwandte Kategorien

Allgemeine Beschreibung

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.

Anwendung

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. Wirkung

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).

Physikalische Form

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

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Persönliche Schutzausrüstung

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

Hier finden Sie alle aktuellen Versionen:

Analysenzertifikate (COA)

Lot/Batch Number
109M4834V
21190824
106M4799V
108K4753

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In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

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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