
In a new study in this issue of PLoS Biology, Youle and colleagues address the question of how Parkin recognises damaged mitochondria, and they find a crucial role for PINK1.ĭamaged mitochondria cannot maintain the potential difference across their inner membrane. The mitochondrial membrane protein PINK1 is also mutated in some forms of familial Parkinson's disease. Recent work showed that the protein Parkin, which is mutated in some forms of familial Parkinson's disease, is recruited from the cytoplasm to damaged mitochondria and that this leads to the breakdown of the mitochondria by processes acting within the cell (autophagy). The neurons of the substantia nigra, which are specifically lost in Parkinson's disease, seem to be especially vulnerable to the effects of mitochondrial damage. Research into the causes of both sporadic and familial Parkinson's disease have led to the idea that a key risk factor might be mitochondrial dysfunction. Biochim Biophys Acta Mol Basis Dis 1867:166104 (2021).PINK1 (labeled in green by GFP, top panels) accumulates on mitochondria (labeled in red with mitotracker, bottom panels) when they are uncoupling with CCCP for 60 minutes or otherwise impaired, signalling mitochondrial dysfunction to Parkin, which triggers their elimination. SUMOylation of mitofusins: A potential mechanism for perinuclear mitochondrial congression in cells treated with mitochondrial stressors. An integrated genomic approach to dissect the genetic landscape regulating the cell-to-cell transfer of a-synuclein. Psiadin and plectranthone selectively inhibit colorectal carcinoma cells proliferation via modulating cyclins signaling and apoptotic pathways. Functional role and molecular mechanisms underlying prohibitin 2 in platelet mitophagy and activation. Unique metabolic phenotype and its transition during maturation of juvenile male germ cells. Publishing research using ab141229? Please let us know so that we can cite the reference in this datasheet.Īb141229 has been referenced in 11 publications.
