ATP13A2 polyclonal antibody
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Specification
Product Description
Rabbit polyclonal antibody raised against synthetic peptide of ATP13A2.
Immunogen
A synthetic peptide corresponding to amino acids 200-300 of human ATP13A2.
Host
Rabbit
Reactivity
Human, Mouse
Form
Liquid
Quality Control Testing
Antibody Reactive Against Synthetic Peptide.
Recommend Usage
Western Blot (2 ug/mL)
Immunohistochemistry (10-20 ug/mL)
The optimal working dilution should be determined by the end user.Storage Buffer
In Tris-glycine, 150 mM NaCl (0.05% sodium azide)
Storage Instruction
Store at -20°C or -80°C.
Aliquot to avoid repeated freezing and thawing.Note
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
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Applications
Western Blot (Tissue lysate)
Western blot analysis of ATP13A2 in mouse brain membrane lysate ATP13A2 polyclonal antibody (Cat # PAB12479).Immunohistochemistry
Staining of ATP13A2 on human brain neurons and neuropils using ATP13A2 polyclonal antibody (Cat # PAB12479) at 10 ug/mL . -
Gene Info — ATP13A2
Entrez GeneID
23400Protein Accession#
Q9NQ11Gene Name
ATP13A2
Gene Alias
FLJ26510, HSA9947, KRPPD, PARK9
Gene Description
ATPase type 13A2
Gene Ontology
HyperlinkGene Summary
This gene encodes a member of the P5 subfamily of ATPases which transports inorganic cations as well as other substrates. Mutations in this gene are associated with Kufor-Rakeb syndrome (KRS), also referred to as Parkinson disease 9. Multiple transcript variants encoding different isoforms have been found for this gene
Other Designations
OTTHUMP00000002399|putative ATPase
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Interactome
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Disease
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Publication Reference
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Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase.
Ramirez A, Heimbach A, Grundemann J, Stiller B, Hampshire D, Cid LP, Goebel I, Mubaidin AF, Wriekat AL, Roeper J, Al-Din A, Hillmer AM, Karsak M, Liss B, Woods CG, Behrens MI, Kubisch C.
Nature Genetics 2006 Oct; 38(10):1184.
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Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase.
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