The threshold for polyglutamine-expansion protein aggregation and cellular toxicity is dynamic and influenced by aging in Caenorhabditis elegans

By James F Morley, Heather R. Brignull, Jill J. Weyers, Richard I. Morimoto. Proceedings of the National Academy of Sciences of the United States of America, 2002

839 citations recorded by the source corpus.

Subfields: Aging, Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/29d245678e64e0cf2ac605b1268eb9a00cf7229c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

1. F. Hartl
2. C. Kenyon
3. Richard I. Morimoto
4. M. Haigis
5. L. Guarente
6. Anat Ben-Zvi
7. E. Miller
8. G. Lithgow

In Cellular and Molecular Neuroscience

1. Richard I. Morimoto
2. F. Hartl
3. C. Kenyon
4. Norbert Perrimon
5. L. Guarente
6. Fabio Demontis

In Molecular Biology

1. Richard I. Morimoto
2. F. Hartl
3. C. Kenyon
4. Anat Ben-Zvi
5. E. Miller
6. M. Haigis
7. G. Jayaraj
8. C. L. Klaips

Citations in the corpus

• Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “Webb & Brunet (2014) have recently unveiled the role of FOXOs as prolongevity factors through the maintenance of protein homeostasis (proteostasis) (Morley et al., 2002; Hsu et al., 2003).”
• 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.”
• Pathways of cellular proteostasis in aging and disease (2018, background): “Aging cells are also less able to cope with and dispose of amyloid-like aggregates (Morley et al., 2002), as exemplified by the fact that cellular aggregate deposits persist although they are typically associated with ubiquitin (Lowe et al.”
• FOXO/4E-BP Signaling in Drosophila Muscles Regulates Organism-wide Proteostasis During Aging (2010, background): “…and Huntington’s disease proteins (proteotoxicity) in C. elegans and mice, suggesting that regulating protein homeostasis (proteostasis) during aging may have a direct effect on the pathogenesis of human neurodegenerative diseases (Cohen et al., 2006; Hsu et al., 2003; Morley et al., 2002).”
• Widespread Protein Aggregation as an Inherent Part of Aging in C. elegans (2010, background): “Muscle KIN-19 Aggravates Paralysis Caused by Polyglutamine Repeats Expressing disease-associated aggregation-prone proteins such as polyglutamine-repeat proteins in the muscle paralyzes the animal as it ages [42,55].”
• Mammalian sirtuins--emerging roles in physiology, aging, and calorie restriction. (2006, background): “One study shows that neurotoxicity in worms is spared by the age-1 mutation , which reduces insulin-like signaling (Morley et al. 2002), or in a transgenic strain overexpressing sir-2.”
• Regulation of longevity in Caenorhabditis elegans by heat shock factor and molecular chaperones. (2003, background): “We have previously demonstrated that the reduced rate of aging in age-1 mutant animals is associated with delayed aggregation and toxicity of polyglutamine expansions that underlie Huntington's Disease and at least eight other matureonset neurodegenerative disorders (Morley et al., 2002 ).”