Cellular defenses against unfolded proteins: a cell biologist thinks about neurodegenerative diseases.

By M. Sherman, A. Goldberg. Neuron, 2001

1,026 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/290ef12cc2a05c0e2c3457d885333a4e96d29cf7

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Citations in the corpus

Altered proteasomal function in sporadic Parkinson's disease. (2003, background): “The ubiquitin-proteasome system (UPS) is the primary biochemical pathway responsible for the degradation of normal and abnormal intracellular proteins, and its failure leads to protein accumulation and cell death (10, 11).”
Parkinson's Disease Mechanisms and Models (2003, background): “…-synuclein may be trafficking proteins to the plasma membrane, as sug- and targets misfolded proteins to the proteasome for degradation (reviewed by Sherman and Goldberg, 2001).gested by the demonstration that -synuclein could be involved in the membrane localization of DAT (Lee et The upstream…”
ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats. (2002, background): “These observations suggest a functional link between proteasomal dysfunction and accumulation of misfolded proteins in the context of polyQ-induced neurotoxicity (Orr 2001; Sherman and Goldberg 2001).”
Protein carbonylation, cellular dysfunction, and disease progression (2006, background): “Just as the aberrant behaviour of enzymes can cause metabolic diseases, the aberrant behaviour of the chaperones and other machinery regulating polypeptide conformations can contribute to misfolding and aggregation diseases [64–66].”
“Sleeping Beauty”: Quiescence in Saccharomyces cerevisiae (2004, background): “(139), although the exact mechanism of neurotoxicity is not”