PARK7 (Protein deglycase DJ-1, Parkinson disease protein 7) is a peptidase of the C56 family that is responsible for inhibiting alpha-synuclein aggregation. It helps protect cells against oxidative stress and cell death. It is also required for correct mitochondrial morphology and function and for autophagy of dysfunctional mitochondria. In the brain, PARK7 regulates the inflammatory response in astrocytes and may regulate lipid raft-dependent endocytosis in astrocytes and neuronal cells. PARK7 is implicated in the pathogenesis of Parkinson’s disease, where it is upregulated in reactive astrocytes. Mutations in PARK7 are a direct cause of early-onset recessive forms of the disease. Such mutations disrupt lipid raft assembly and lead to impaired glutamate uptake and are associated with Lewy body pathology. Loss of function or knockout of PARK7 also leads to a limited ability of astrocytes to protect neurons from neurotoxicity. In immunohistochemistry, PARK7 has cytoplasmic and nuclear positivity in most tissues throughout the body. References: Mol. Genet. 2013;22:4805–4817, PMID: 23847046; J. Neurochem. 2011;117:375–387, PMID: 21219333; Trends Neurosci. 2017 Jun; 40(6): 358–370, PMID: 28527591; Brain. 2016. 139 (6), 1680–1687:10.1093/brain/aww080