The roles of intracellular protein-degradation pathways in neurodegeneration

By D. Rubinsztein. Nature, 2006

1,713 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/cc10ae62d5dec5d897ebdd3fdc33325e1b16ff26

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Citations in the corpus

Persistent activation of Nrf2 through p62 in hepatocellular carcinoma cells (2011, background): “Macroautophagy (hereafter referred to as autophagy) is a cellular degradation system in which cytoplasmic components, including organelles, are sequestered by double membrane structures called autophagosomes and the sequestered materials are degraded by lysosomal hydrolases for supply of amino acids”
FOXO/4E-BP Signaling in Drosophila Muscles Regulates Organism-wide Proteostasis During Aging (2010, background): “…factor FOXO and its target Thor/4E-BP are sufficient to delay this process and preserve muscle function at least in part by promoting the basal activity of the autophagy/lysosome system, an intracellular protein degradation pathway that removes damaged protein aggregates (Rubinsztein, 2006).”
Lysosomal Proteolysis and Autophagy Require Presenilin 1 and Are Disrupted by Alzheimer-Related PS1 Mutations (2010, neutral): “…major lysosomal degradative pathway in cells, is responsible for degrading long-lived cytoplasmic constituents and is the principal mechanism for turning over cellular organelles and protein aggregates too large to be degraded by the proteasome (Klionsky, 2007; Mizushima, 2007; Rubinsztein, 2006).”
Tau Protein Hyperphosphorylation and Aggregation in Alzheimer’s Disease and Other Tauopathies, and Possible Neuroprotective Strategies (2016, background): “In the case of soluble monomeric or small oligomeric tau protein, the endocytosis appears to be clathrin-dependent (reviewed in [169]).”
The Nucleolus under Stress (2010, neutral): “At this stage, it is tempting to draw a parallel with the proteasome impairment observed in several neurodegenerative diseases, such as Huntington's or Parkinson's, which leads to the accumulation of misfolded proteins in nuclear aggregates (Rubinsztein, 2006) .”
Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “On the other hand, there are studies suggesting that aggregates themselves might actually serve a neuroprotective function (Arrasate et al., 2004; Rubinsztein, 2006).”
Role of autophagy in cancer (2007, background): “Protein turnover by lysosomal degradation through the autophagy pathway is functionally coupled to, and compensatory with, the ubiquitin-mediated proteasome protein degradation pathwa”
Autophagy-deficient mice develop multiple liver tumors. (2011, background): “…starvation, quality control of intracellular proteins and organelles, preimplantation embryonic development, elimination of intracellular microbes, and presentation of cytoplasmic antigens (Rubinsztein 2006; Mizushima 2007; Cecconi and Levine 2008; Mizushima et al. 2008; Deretic and Levine 2009).”
Toll‐like receptors control autophagy (2008, background): “effect on a wide range of normal physiological processes, including ageing and diseases such as cancer (Levine, 2007) and neurodegeneration (Alzheimer’s, Huntington’s and Parkinson’s diseases and ataxias; Rubinsztein, 2006).”
Connecting endoplasmic reticulum stress to autophagy by unfolded protein response and calcium (2007, positive): “Huntington’s disease with polyQ aggregates and Parkinson’s disease with a-synuclein aggregates) suggest that the ER stress-induced autophagy enhances the removal of aggregates (in this case cytosolic aggregates) and enhances cell survival.(25,56) Accordingly, pharmacological TOR inhibitors protect a”