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Wichtige Dokumente
A3361
Anti-ATP13A2 (C-terminal region) antibody produced in rabbit
~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
Empfohlene Produkte
Biologische Quelle
rabbit
Qualitätsniveau
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: 1.5-3.0 μg/mL using mouse brain extract (S1 fraction) or HEK-293T cells expressing human ATP13A2
UniProt-Hinterlegungsnummer
Versandbedingung
dry ice
Lagertemp.
−20°C
Posttranslationale Modifikation Target
unmodified
Angaben zum Gen
human ... ATP13A2(23400)
Allgemeine Beschreibung
ATP13A2 (ATPase type 13A2, also known as PARK9) is a neuronal P-type ATPase of the P5 subfamily. It is present in the lysosome of transiently transfected cells, whereas the unstable truncated mutants are retained in the endoplasmic reticulum and degraded by the proteasome.
ATP13A2 is a member of the P5 subfamily of P-type transport ATPases which include ATP13A1-ATP13A5. Mutations in ATP3A2 also known as PARK9 are associated with hereditary Parkinson′s disease.
Rabbit anti-ATP13A2 (C-terminal region) antibody is specific for human and mouse ATP13A2. Staining of the ATP13A2 band by immunoblotting is specifically inhibited by the ATP13A2 immunizing peptide.
Anwendung
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)
Western Blotting (1 paper)
Rabbit anti-ATP13A2 (C-terminal region) antibody has been used for western blotting applications at a dilution of 1:1000.
Biochem./physiol. Wirkung
ATP13A2 (ATPase type 13A2, also known as PARK9) shows elevated expression levels in the brains of sporadic Parkinson′s disease (PD) patients, suggesting a potential role in the more common forms of PD. It is associated with Kufor-Rakeb syndrome (KRS). KRS is a rare form of hereditary PD with juvenile onset. In addition to typical signs of PD, affected individuals show symptoms of more widespread pyramidal neurodegeneration, including dementia.
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
12 - Non Combustible Liquids
WGK
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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)
Alejandra Lucía Marcos et al.
Biochimica et biophysica acta. Biomembranes, 1861(10), 182993-182993 (2019-05-28)
Mutations in the ATP13A2 gene (PARK9, CLN12, OMIM 610513) were initially associated with a form of Parkinson's Disease (PD) known as Kufor Rakeb Syndrome (KRS). However, the genetic spectrum of ATP13A2-associated disorders was expanded in the last years, because it
Shaun Martin et al.
Parkinson's disease, 2016, 9531917-9531917 (2016-04-14)
The late endo-/lysosomal P-type ATPase ATP13A2 (PARK9) is implicated in Parkinson's disease (PD) and Kufor-Rakeb syndrome, early-onset atypical Parkinsonism. ATP13A2 interacts at the N-terminus with the signaling lipids phosphatidic acid (PA) and phosphatidylinositol (3,5) bisphosphate (PI(3,5)P2), which modulate ATP13A2 activity
Alejandro Estrada-Cuzcano et al.
Brain : a journal of neurology, 140(2), 287-305 (2017-02-01)
Hereditary spastic paraplegias are heterogeneous neurodegenerative disorders characterized by progressive spasticity of the lower limbs due to degeneration of the corticospinal motor neurons. In a Bulgarian family with three siblings affected by complicated hereditary spastic paraplegia, we performed whole exome
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
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