Opposing Activities Protect Against Age-Onset Proteotoxicity

By E. Cohen, J. Bieschke, Rhonda M. Perciavalle, J. Kelly, A. Dillin. Science, 2006

896 citations recorded by the source corpus.

Subfields: Aging, Endocrine and Autonomic Systems, Physiology

View Paper: https://www.semanticscholar.org/paper/008c0e372f7fc4ad52a144b7c491560b00a6dfdc

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In Aging

In Endocrine and Autonomic Systems

In Physiology

Citations in the corpus

Direct Observation of the Interconversion of Normal and Toxic Forms of α-Synuclein (2012, background): “Indeed, our results support the hypothesis that fibrils can act either to sequester misfolded potentially toxic species (Lansbury, 1999) or, depending on the conditions, to release them into the local environment, thereby unifying two apparently distinct views drawn from observations of protein aggr”
Collapse of proteostasis represents an early molecular event in Caenorhabditis elegans aging (2009, methodology): “Animals were stained with rhodamine phalloidin (Molecular Probes) and with either anti-paramyosin [5-23] (57), anti-myosin heavy chain B [28.”
The tip of the iceberg: RNA-binding proteins with prion-like domains in neurodegenerative disease (2012, background): “Recently, however, the mammalian protein disaggregase machinery comprising Hsp110, Hsp70 and Hsp40 has been revealed (Shorter, 2011), and additional disaggregases are also likely to contribute to metazoan proteostasis (Bieschke et al., 2009; Cohen et al., 2006).”
A century-old debate on protein aggregation and neurodegeneration enters the clinic (2006, background): “assemble in a stepwise process involving low-molecular-weight oligomers, the relative importance of these is difficult to assess because they are too unstable to characteriz”
Molecular chaperones in protein folding and proteostasis (2011, background): “A plausible explanation for the late onset of these diseases is provided by recent evidence from model organisms that the signalling pathways that regulate proteostasis are integrated with the genetic and epigenetic pathways that control longevit”
The high-affinity HSP90-CHIP complex recognizes and selectively degrades phosphorylated tau client proteins. (2007, background): “An additional potential mechanism, however, is age-associated loss of activity and expression of chaperone and associated proteins (35).”
Widespread Protein Aggregation as an Inherent Part of Aging in C. elegans (2010, background): “Why might this be? Many recent studies show that low-MW oligomers formed by diseasemisfolded proteins are at least as, if not more, toxic as high-MW, visible, aggregates [43,84,85,86].”
Alzheimer's disease. (2011, background): “elegans model also suggest that small oligomers of Ab can confer cytotoxicity (Cohen et al. 2006).”