Please use this identifier to cite or link to this item:
|Title:||Novel Monoclonal Antibodies Demonstrate Biochemical Variation of Brain Parkin with Age||Authors:||Pawlyk A.C.
|Issue Date:||2003||Publisher:||American Society for Biochemistry and Molecular Biology||Citation:||Pawlyk A.C., Giasson B.I., Sampathu D.M., Perez F.A., Lim K.L., Dawson V.L., Dawson T.M., Palmiter R.D., Trojanowski J.Q., Lee V.M.-Y. (2003). Novel Monoclonal Antibodies Demonstrate Biochemical Variation of Brain Parkin with Age. Journal of Biological Chemistry 278 (48) : 48120-48128. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.M306889200||Abstract:||Autosomal recessive juvenile parkinsonism is a movement disorder associated with the degeneration of dopaminergic neurons in substantia nigra pars compacta. The loss of functional parkin caused by parkin gene mutations is the most common single cause of juvenile parkinsonism. Parkin has been shown to aid in protecting cells from endoplasmic reticulum and oxidative stressors presumably due to ubiquitin ligase activity of parkin that targets proteins for proteasomal degradation. However, studies on parkin have been impeded because of limited reagents specific for this protein. Here we report the generation and characterization of a panel of parkin-specific monoclonal antibodies. Biochemical analyses indicate that parkin is present only in the high salt-extractable fraction of mouse brain, whereas it is present in both the high salt-extractable and RIPA-resistant, SDS-extractable fraction in young human brain. Parkin is present at decreased levels in the high salt-extractable fraction and at increased levels in the SDS-extractable fraction from aged human brain. This shift in the extractability of parkin upon aging is seen in humans but not in mice, demonstrating species-specific differences in the biochemical characteristics of murine versus human parkin. Finally, by using these highly specific anti-parkin monoclonal antibodies, it was not possible to detect parkin in ?-synuclein-containing lesions in ? -synucleinopathies thereby challenging prior inferences about the role of parkin in movement disorders other than autosomal recessive juvenile parkinsonism.||Source Title:||Journal of Biological Chemistry||URI:||http://scholarbank.nus.edu.sg/handle/10635/150217||ISSN:||219258||DOI:||10.1074/jbc.M306889200|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
|jbc.M306889200.pdf||523.99 kB||Adobe PDF|
checked on Jul 4, 2020
WEB OF SCIENCETM
checked on Dec 31, 2018
checked on Jul 3, 2020
checked on Jul 3, 2020
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.