Cellular clearance of circulating transthyretin decreases cell-nonautonomous proteotoxicity in Caenorhabditis elegans

Cell-autonomous and cell-nonautonomous mechanisms of neuro-degeneration appear to occur in the proteinopathies, including Alzheimer’s and Parkinson’s diseases. However, how neuronal toxicity is generated from misfolding-prone proteins secreted by nonneuronal tissues and whether modulating protein ag...

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 2018-08, Vol.115 (33), p.E7710-E7719
Hauptverfasser:	Madhivanan, Kayalvizhi, Greiner, Erin R., Alves-Ferreira, Miguel, Soriano-Castell, David, Rouzbeh, Nirvan, Aguirre, Carlos A., Paulsson, Johan F., Chapman, Justin, Jiang, Xin, Ooi, Felicia K., Lemos, Carolina, Dillin, Andrew, Prahlad, Veena, Kelly, Jeffery W., Encalada, Sandra E.
Format:	Artikel
Sprache:	eng
Schlagworte:	Amyloid Neuropathies - genetics Amyloid Neuropathies - metabolism Animal models Animals Animals, Genetically Modified Biological Sciences Caenorhabditis elegans Caenorhabditis elegans - cytology Caenorhabditis elegans - genetics Caenorhabditis elegans - metabolism Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - metabolism Cellular biology Degeneration Degradation Humans Macrophages Muscles Neurodegeneration Neurogenesis Neurons Neurotoxicity Pain perception Peripheral neuropathy Pharmacology PNAS Plus Prealbumin - genetics Prealbumin - metabolism Protein Aggregates Protein Aggregation, Pathological - genetics Protein Aggregation, Pathological - metabolism Protein folding Proteins RNA-mediated interference Sensory neurons Toxicity Transthyretin
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