The ubiquitin proteasome system in neurodegenerative diseases: sometimes the chicken, sometimes the egg.

By Aaron Ciechanover, P. Brundin. Neuron, 2003

995 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/6eb4d38e99e9910ea77f37c75759ca0fa0951eb0

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Citations in the corpus

The high-affinity HSP90-CHIP complex recognizes and selectively degrades phosphorylated tau client proteins. (2007, methodology): “Using this model, we have previously shown that CHIP–/– mice have increased p-tau (14).”
Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “Moreover, pathogenesis of neurodegenerative disorders such as Parkinson’s, Alzheimer’s, or Huntington’s disease is generally related to an abnormal ubiquitinproteasome mechanism as either a primary cause or secondary consequence (Ciechanover & Brundin, 2003; Kikis et al., 2010; Webb & Brunet, 2014).”
Mitochondrial Dysfunction in Parkinson's Disease (2011, background): “Dysfunction of protein metabolism appears to be an important factor in LB formation and the associated neurodegeneration (see for further review [137]), but the significance of these aggregates is still a subject of debate.”
Oxidative stress and neurodegeneration: where are we now? (2006, background): “However, most attention has been paid to the proteasome, a cytoplasmic and nuclear system in eukaryotic cells that removes unwanted proteins, including iKB, hypoxiainducible factor-1a, phosphorylated catalase, cyclins, Keap1 and oxidatively damaged proteins (McNaught et al. 2001; Ciechanover and Bru”
Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice (2005, background): “A growing number of disease-associated proteins have been found to accumulate in aggresome, including huntingtin, parkin, -synuclein, and peripheral myelin protein 22 (Notterpek et al., 1999; Ciechanover and Brundin, 2003).”
Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration (2007, background): “Proteins targeted for degradation are ubiquitinated and several hallmark inclusions in neurodegenerative disease either in neurons or glia or both are detected by ubiquitin IHC [17, 19, 47, 48].”
ER stress and neurodegenerative diseases (2006, background): “tion of proteins in the cell leading also to ER stress and aggravation of the disease.(4,5,9) To this come effects of environmental toxins, reactive oxygen species (ROS) and”
Broad activation of the ubiquitin–proteasome system by Parkin is critical for mitophagy (2011, background): “By linking Parkin-mediated polyubiquitination to the UPS, our results support, in a general sense, earlier models postulating a role for Parkin in cellular protein quality control (14).”
Intravesicular Localization and Exocytosis of α-Synuclein and its Aggregates (2005, background): “Furthermore, mitochondrial and proteasomal dysfunctions, conditions that are associated with intracellular -syn aggregation and pathogenesis of PD (Ciechanover and Brundin, 2003; Lee, 2003), caused elevated secretion of -syn aggregates.”
Oxidative stress in neurodegenerative diseases (2012, background): “Such phenomena have been implicated in many oxidative stress-associated disorders, including neurodegenerative diseases [63-64] .”
Sequestosome 1/p62 Is a Polyubiquitin Chain Binding Protein Involved in Ubiquitin Proteasome Degradation (2004, background): “The role of aggregates and their relationship to cell survival are controversial (1, 6).”