Cell Signaling Technology

Product Pathways - Neuroscience

PARK9 Antibody #5879

Applications Reactivity Sensitivity MW (kDa) Source
W IP H M R Mk Endogenous 150 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

PARK9 Antibody recognizes endogenous levels of total PARK9 protein.

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.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa and COS-7 cells using PARK9 Antibody.

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 (5,6).

  1. Fahn, S. (2003) Ann N Y Acad Sci 991, 1-14.
  2. Moore, D.J. et al. (2005) Annu Rev Neurosci 28, 57-87.
  3. Ramirez, A. et al. (2006) Nat Genet 38, 1184-91.
  4. Xiromerisiou, G. et al. (2010) Neurosurg Focus 28, E7.
  5. Klein, C. and Lohmann-Hedrich, K. (2007) Curr Opin Neurol 20, 453-64.
  6. Xiromerisiou, G. et al. (2010) Neurosurg Focus 28, E7.

Application References

Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know!

Companion Products

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

Products