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Your search keyword '"Steinkraus, Katherine A."' showing total 3 results
Start Over Author "Steinkraus, Katherine A." Topic caenorhabditis elegans
3 results on '"Steinkraus, Katherine A."'

1. Proteasomal regulation of the hypoxic response modulates aging in C. elegans.

Author

Mehta R, Steinkraus KA, Sutphin GL, Ramos FJ, Shamieh LS, Huh A, Davis C, Chandler-Brown D, and Kaeberlein M

Subjects
Amyloid beta-Peptides toxicity, Animals, Caenorhabditis elegans genetics, Caenorhabditis elegans metabolism, Caenorhabditis elegans Proteins genetics, Caloric Restriction, Cullin Proteins genetics, Female, Fertility, Gene Expression Regulation, Homeostasis, Insulin metabolism, Longevity physiology, Male, Models, Animal, Peptides toxicity, RNA Interference, Receptor, Insulin genetics, Receptor, Insulin metabolism, Signal Transduction, Transcription Factors genetics, Ubiquitination, Aging physiology, Caenorhabditis elegans physiology, Caenorhabditis elegans Proteins metabolism, Cullin Proteins metabolism, Oxygen physiology, Proteasome Endopeptidase Complex metabolism, Transcription Factors metabolism
Abstract

The Caenorhabditis elegans von Hippel-Lindau tumor suppressor homolog VHL-1 is a cullin E3 ubiquitin ligase that negatively regulates the hypoxic response by promoting ubiquitination and degradation of the hypoxic response transcription factor HIF-1. Here, we report that loss of VHL-1 significantly increased life span and enhanced resistance to polyglutamine and beta-amyloid toxicity. Deletion of HIF-1 was epistatic to VHL-1, indicating that HIF-1 acts downstream of VHL-1 to modulate aging and proteotoxicity. VHL-1 and HIF-1 control longevity by a mechanism distinct from both dietary restriction and insulin-like signaling. These findings define VHL-1 and the hypoxic response as an alternative longevity and protein homeostasis pathway.

Published
2009
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2. Dietary restriction suppresses proteotoxicity and enhances longevity by an hsf-1-dependent mechanism in Caenorhabditis elegans.

Author

Steinkraus KA, Smith ED, Davis C, Carr D, Pendergrass WR, Sutphin GL, Kennedy BK, and Kaeberlein M

Subjects
Animals, Caenorhabditis elegans drug effects, Caenorhabditis elegans genetics, Caenorhabditis elegans Proteins drug effects, Food Deprivation physiology, Longevity drug effects, Peptides pharmacology, Transcription Factors drug effects, Caenorhabditis elegans metabolism, Caenorhabditis elegans Proteins metabolism, Caloric Restriction, Longevity physiology, Transcription Factors metabolism
Abstract

Dietary restriction increases lifespan and slows the onset of age-associated disease in organisms from yeast to mammals. In humans, several age-related diseases are associated with aberrant protein folding or aggregation, including neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's diseases. We report here that dietary restriction dramatically suppresses age-associated paralysis in three nematode models of proteotoxicity. Similar to its longevity-enhancing properties, dietary restriction protects against proteotoxicity by a mechanism distinct from reduced insulin/IGF-1-like signaling. Instead, the heat shock transcription factor, hsf-1, is required for enhanced thermotolerance, suppression of proteotoxicity, and lifespan extension by dietary restriction. These findings demonstrate that dietary restriction confers a general protective effect against proteotoxicity and promotes longevity by a mechanism involving hsf-1.

Published
2008
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3. Dietary restriction suppresses proteotoxicity and enhances longevity by an hsf-1-dependent mechanism in C. elegans

Author

Steinkraus, Katherine A., Smith, Erica D., Davis, Christina, Carr, Daniel, Pendergrass, William R., Sutphin, George L., Kennedy, Brian K., and Kaeberlein, Matt

Subjects
Longevity, Animals, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Food Deprivation, Peptides, Article, Caloric Restriction, Transcription Factors
Abstract

Dietary restriction increases life span and slows the onset of age-associated disease in organisms from yeast to mammals. In humans, several age-related diseases are associated with aberrant protein folding or aggregation, including neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. We report here that dietary restriction dramatically suppresses age-associated paralysis in three nematode models of proteotoxicity. Similar to its longevity-enhancing properties, dietary restriction protects against proteotoxicity by a mechanism distinct from reduced insulin/IGF-1-like signaling. Instead, the heat shock transcription factor, hsf-1, is required for enhanced thermotolerance, suppression of proteotoxicity, and life span extension by dietary restriction. These findings demonstrate that dietary restriction confers a general protective effect against proteotoxicity and promotes longevity by a mechanism involving hsf-1.

Published
2008

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