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Hoepken, H.H., Gispert, S., Morales, B., et al. (2007) Mitochondrial Dysfunction, Peroxidation Damage and Changes in Glutathione Metabolism in PARK6. Neurobiology of Disease, 25, 401-411.
http://dx.doi.org/10.1016/j.nbd.2006.10.007

has been cited by the following article:

  • TITLE: Pink1 Rescues Gal4-Induced Developmental Defects in the Drosophila Eye

    AUTHORS: Amy M. Todd, Brian E. Staveley

    KEYWORDS: Drosophila melanogaster, Pink1, Parkin, Gal4, Toxic Protein, Parkinson Disease

    JOURNAL NAME: Advances in Parkinson's Disease, Vol.4 No.3, July 23, 2015

    ABSTRACT: Parkinson disease pathology often includes the presence of ubiquitin-positive, α-synuclein-enriched inclusions in the remaining neurons. Pink1 (also identified as PARK6) encodes a serinethreonine kinase involved in mitochondrial protection that works with parkin to ubiquitinate various proteins, promoting mitophagy. The parkin protein works to tag cystolic proteins for degradation, and previous work in our laboratory has shown the ability of parkin to rescue a Gal4-induced phenotype. To further investigate the role of Pink1 in protection against toxic proteins, we have performed expression studies to determine the effects of increases and decreases in Pink1 on the Gal4-induced phenotype consisting of developmental defects in the Drosophila eye. Our results show that Pink1 is able to rescue the Gal4-induced phenotype, highlighting a protective role for Pink1 against toxic proteins. When expressing low levels of Gal4, reductions in Pink1 or parkin are not able to induce a phenotype. This suggests that Pink1 or parkin may counter Gal4 effects despite reductions, or that the effects of low level Gal4 may be alleviated by an alternative mechanism. Moreover, the Pink1 mechanism of action during differing types of cell stress, including degradation of toxic proteins, warrants further investigation.