Developed in collaboration with The Michael J. Fox Foundation, this model contains a deletion of the Park2 (Parkinson disease [autosomal recessive, juvenile] 2) gene, encoding for the protein Parkin. Mutations in Parkin have been linked to early-onset Parkinson’s disease (PD), making this model useful to further understand the role of Parkin in PD.
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Figure 1. Loss of Parkin protein in Park2 knockout rats
Parkin protein expression is disrupted in Park2 knockout rats as compared to wild type controls as demonstrated by Western blot.
Figure 2. Rotarod performance of Park2 knockout rats at 12 months of age
Park2 knockout animals show no deficits in motor activity as assessed by rotarod at 12 months of age.
In humans, loss of function of Park2 leads to a form of familial Parkinson's disease. The Parkin protein is part of the ubiquitin-proteasomal enzyme pathway and may help degrade other proteins that are toxic to neurons. Roughly 20% of patients with Parkinson's disease onset before age 40 have mutations within Park2, making this an ideal model for the study of Parkinson's disease.
