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Render Timestamp: 2024-07-26T10:51:09.004Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

PARK9 Antibody #5879

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 150
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    PARK9 Antibody recognizes endogenous levels of total PARK9 protein.


    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser282 of human PARK9 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    Parkinson’s disease (PD), the second most common neurodegenerative disease after Alzheimer’s, is a progressive movement disorder characterized by rigidity, tremors and postural instability. The pathological hallmark of PD is progressive loss of dopaminergic neurons in the substantia nigra of the ventral midbrain and the presence of intracellular Lewy bodies (protein aggregates of α-synuclein, ubiquitin and other components) in surviving neurons of the brain stem (1). Various genes and loci (α-synuclein/PARK1 and 4, parkin/PARK2, UCH-L1/PARK5, PINK1/PARK6, DJ-1/PARK7, LRRK2/PARK8, ATP13A2/PARK9) are genetically linked to PD (2).

    PARK9, also known as ATP13A2, is a member of the P-type ATPase superfamily and is involved in the lysosomal degradation pathway, clearing α-synuclein aggregates (3,4). The protein has 10 transmembrane domains and wild-type PARK9 localizes to the lysosomal membrane. In contrast, all three known mutations, which have premature stop codons resulting in a truncated protein, are retained in the endoplasmic reticulum and degraded by the proteasome. PARK9 is predominantly expressed in the brain and has been linked to Kufor-Rakeb Syndrome, a monogenic form of recessively inherited, atypical parkinsonism that is characterized by juvenile-onset, with pyramidal degeneration and cognitive dysfunction (4,5).

    For Research Use Only. Not For Use In Diagnostic Procedures.
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