A3361
Anti-ATP13A2 (C-terminal region) antibody produced in rabbit
~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
Produits recommandés
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: 1.5-3.0 μg/mL using mouse brain extract (S1 fraction) or HEK-293T cells expressing human ATP13A2
Numéro d'accès UniProt
Conditions d'expédition
dry ice
Température de stockage
−20°C
Modification post-traductionnelle de la cible
unmodified
Informations sur le gène
human ... ATP13A2(23400)
Catégories apparentées
Description générale
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.
Application
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.
Actions biochimiques/physiologiques
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.
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
12 - Non Combustible Liquids
Classe de danger pour l'eau (WGK)
nwg
Certificats d'analyse (COA)
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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.
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
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)
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
Mark Ainsley Colijn et al.
Neurogenetics (2024-07-18)
Biallelic (autosomal recessive) pathogenic variants in ATP13A2 cause a form of juvenile-onset parkinsonism, termed Kufor-Rakeb syndrome. In addition to motor symptoms, a variety of other neurological and psychiatric symptoms may occur in affected individuals, including supranuclear gaze palsy and cognitive
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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