Expanding insights of mitochondrial dysfunction in Parkinson's disease

By P. Abou-Sleiman, M. Muqit, N. Wood. Nature Reviews Neuroscience, 2006

912 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/c0c687fbc89c9c8c157725a9180a3926858c8905

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Citations in the corpus

Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy. (2010, background): “Genes associated with familial forms of PD further support the role of mitochondria and protein quality control in disease pathogenesis (9), in particular, the PINK1, Parkin and ATP13A2 genes, which encode for a mitochondrially targeted serine/threonine kinase, an E3 ubiquitin-protein ligase and a l”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “…oxygen species (ROS), which damage mtDNA, components of the respiratory chain and other mitochondrial factors, thereby triggering a vicious circle between mitochondrial impairment and oxidative stress (reviewed in Abou-Sleiman et al , 2006; Lin and Beal, 2006; and Henchcliffe and Beal, 2008).”
Diagnosis and treatment of Parkinson disease: molecules to medicine. (2006, background): “A common feature of sporadic PD is evidence of complex I mitochondrial dysfunction (119).”
PINK1 is activated by mitochondrial membrane potential depolarization and stimulates Parkin E3 ligase activity by phosphorylating Serine 65 (2012, background): “Given the large body of evidence implicating mitochondrial dysfunction in PD [26], it would be important to explore in subsequent work whether Ser(65) and perhaps Thr(257) phosphorylation could have utility as specific biomarkers for PD progression.”
Mitochondrial membrane permeabilization in cell death. (2007, background): “Thus, at present, there is no genetic evidence suggesting that Omi/HtrA2 or Smac/DIABLO would contribute to cell death in vivo.”
Calcium and neurodegeneration (2007, background): “…al ., 2001; Drew & Leeuwenburgh, Calcium and neurodegeneration, M. P. Mattson © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2007 No claim to original US government works 339 & Ischiropoulos, 2005; Saito et al ., 2005; Abou-Sleiman et al ., 2006; Mattson & Magnus, 2006).”
Enriched environments, experience-dependent plasticity and disorders of the nervous system (2006, neutral): “Various PD-associated genes have recently been identified, including α-synuclein , parkin , PINK1 (phosphatase and tensin homologue (PTEN)-induced kinase 1), DJ1 (Parkinson disease (autosomal recessive, early onset) 7) and LRRK2 (leucine-rich repeat kinase 2) (for a review, see Ref”
Pink1, Parkin, DJ-1 and mitochondrial dysfunction in Parkinson's disease. (2007, background): “Mutant SNCA expression also increases sensitivity to inhibitors of mitochondrial complex I, whereas loss-of-function of a-Synuclein promotes resistance to these compounds [51].”
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy (2008, background): “Although Parkin function has been implicated in several cellular functions, study of Parkin loss in model organisms suggests that Parkin may have a conserved role in maintaining mitochondrial function and integrity ( Abou-Sleiman et al., 2006 ; Hardy et al., 2006 ).”
Visualizing stromal cell dynamics in different tumor microenvironments by spinning disk confocal microscopy (2008, background): “Mitochondrial dysfunction has recently been highlighted as a potential, common disease mechanism in PD linking environmental, genetic and age-related influences (Abou-Sleiman et al., 2006; Mandemakers et al., 2007).”
Mitochondrial processing peptidase regulates PINK1 processing, import and Parkin recruitment (2012, background): “Several lines of evidence implicate mitochondrial dysfunction in PD [2], including the role of two recessive PD genes, Parkin and phosphatase and tensin homologue-induced putative kinase 1 (PINK1), in a new mitochondrial quality control pathway [3].”