ArticleThe Journal of cell biology2008
Longevity mutation in SCH9 prevents recombination errors and premature genomic instability in a Werner/Bloom model system.
Article in The Journal of cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 65 citations in OpenAlex.
- The Yeast Protein Kinase Sch9 Functions as a Central Nutrient-Responsive Hub That Calibrates Metabolic and Stress-Related Responses.Journal of fungi (Basel, Switzerland) · 2023Review
- Balancing DNA repair to prevent ageing and cancer.Experimental cell research · 2021Review
- Genes affecting the extension of chronological lifespan in Schizosaccharomyces pombe (fission yeast).Molecular microbiology · 2021Review
- Intragenic repeat expansion in the cell wall protein geneGenome research · 2020Article
- Cell organelles and yeast longevity: an intertwined regulation.Current genetics · 2020Review
- Beyond Host Defense: Deregulation ofFrontiers in immunology · 2020Review
- Activating the Anaphase Promoting Complex to Enhance Genomic Stability and Prolong Lifespan.International journal of molecular sciences · 2018Review
- Starvation, Stress Resistance, and Cancer.Trends in endocrinology and metabolism: TEM · 2018Review
- Dietary restriction and lifespan: Lessons from invertebrate models.Ageing research reviews · 2017Review
- Increased levels of RNA oxidation enhance the reversion frequency in aging pro-apoptotic yeast mutants.Apoptosis : an international journal on programmed cell death · 2017Article
- Tethering telomerase to telomeres increases genome instability and promotes chronological aging in yeast.Aging · 2016Article
- Article
- Growth factors, aging and age-related diseases.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2016Article
- Feedback Control of Snf1 Protein and Its Phosphorylation Is Necessary for Adaptation to Environmental Stress.The Journal of biological chemistry · 2015Article
- Protein and amino acid restriction, aging and disease: from yeast to humans.Trends in endocrinology and metabolism: TEM · 2014Review
- Reducing signs of aging and increasing lifespan by drug synergy.Aging cell · 2013Article
- DNA replication stress-induced loss of reproductive capacity in S. cerevisiae and its inhibition by caloric restriction.Cell cycle (Georgetown, Tex.) · 2013Article
- Somatotropic signaling: trade-offs between growth, reproductive development, and longevity.Physiological reviews · 2013Review
- Hrq1 functions independently of Sgs1 to preserve genome integrity in Saccharomyces cerevisiae.Journal of microbiology (Seoul, Korea) · 2013Article
- Aging, nutrient signaling, hematopoietic senescence, and cancer.Critical reviews in oncogenesis · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Werner and Bloom syndromes are human diseases characterized by premature age-related defects including elevated cancer incidence. Using a novel Saccharomyces cerevisiae model system for aging and cancer, we show that cells lacking the RecQ helicase SGS1 (WRN and BLM homologue) undergo premature age-related changes, including reduced life span under stress and calorie restriction (CR), G1 arrest defects, dedifferentiation, elevated recombination errors, and age-dependent increase in DNA mutations. Lack of SGS1 results in a 110-fold increase in gross chromosomal rearrangement frequency during aging of nondividing cells compared with that generated during the initial population expansion. This underscores the central role of aging in genomic instability. The deletion of SCH9 (homologous to AKT and S6K), but not CR, protects against the age-dependent defects in sgs1Delta by inhibiting error-prone recombination and preventing DNA damage and dedifferentiation. The conserved function of Akt/S6k homologues in lifespan regulation raises the possibility that modulation of the IGF-I-Akt-56K pathway can protect against premature aging syndromes in mammals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.