Parkin- An E3 Ubiquitin Ligase with Multiple Substrates
Anna Sandebring* and Angel Cedazo-Mínguez
Karolinska Institutet Department of NVS, KI-Alzheimer’s Disease Research Center, NOVUM floor 5, 141 57 Huddinge, Sweden
- Corresponding Author:
- Anna Sandebring
Karolinska Institutet., Department of NVS
KI-Alzheimerâ€™s Disease Research Center
NOVUM, 141 57 Huddinge, Sweden
Tel: +468 58 58 36 67
Fax: +468 58 58 83 80
E-mail: [email protected]
Received date: march 19, 2012; Accepted date: May 07, 2012; Published date: May 09, 2012
Citation: Sandebring A, Cedazo-MÃnguez A (2012) Parkin- An E3 Ubiquitin Ligase with Multiple Substrates. J Alzheimers Dis Parkinsonism S10:002. doi:10.4172/2161-0460.S10-002
Copyright: © 2012 Sandebring A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Parkinson’s disease is a common neurodegenerative disorder. The clinical symptoms arise from a substantial loss of dopaminergic neurons in substantia nigra pars compacta, which causes motor symptoms such as bradykinesia and tremor. Although the majority of PD cases are sporadic, there is a growing number of genes shown to be involved in causing parkinsonism that manifests with similar pathology to the idiopathic disease. The most common cause to autosomal recessive parkinson’s disease (ARPD) is mutations in the gene encoding for parkin- an E3 ubiquitin ligase with widespread functions in the cell. In this review we summarize the substrates identified for parkin and which functions these imply in the cell. Elucidating the mechanism of functions of these substrates may contribute with clues on which pathways to study further in Parkinson’s disease pathology.