Zobrazeno 1 - 10
of 103
pro vyhledávání: '"E. Gottschling"'
Autor:
Anthony O. Beas, Patricia B. Gordon, Clara L. Prentiss, Carissa Perez Olsen, Matthew A. Kukurugya, Bryson D. Bennett, Susan M. Parkhurst, Daniel E. Gottschling
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-10 (2020)
Age-associated metabolic changes include lipid accumulation. Here, the authors show that with replicative aging yeast accumulate lipid droplets which protect cells from cold stress and can be modulated through Biosynthesis of NAD+ 2 (BNA2).
Externí odkaz:
https://doaj.org/article/ccc42411f0664158949caf4ea685050d
Publikováno v:
eLife, Vol 5 (2016)
Mitochondrial dysfunction is a hallmark of aging, and underlies the development of many diseases. Cells maintain mitochondrial homeostasis through a number of pathways that remodel the mitochondrial proteome or alter mitochondrial content during time
Externí odkaz:
https://doaj.org/article/58fd680ae64c4870a87c5060d7aa9b6e
Autor:
Nathaniel H. Thayer, Michael Robles, Jun Xu, Elizabeth L. Schinski, Manuel Hotz, Robert Keyser, Alfred Millett-Sikking, Voytek Okreglak, Jason V. Rogers, Adam J. Waite, Bernd J. Wranik, Andrew G. York, R. Scott McIsaac, Daniel E. Gottschling
SummaryThe budding yeast, Saccharomyces cerevisiae, has emerged as a model system for studying the aging processes in eukaryotic cells. However, the full complement of tools available in this organism has not been fully applied, in part because of li
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::911620ff6fc9c8d9976a478b2fc7f600
https://doi.org/10.1101/2022.02.14.480146
https://doi.org/10.1101/2022.02.14.480146
Publikováno v:
Molecular Biology of the Cell
Mitochondrial decline is a hallmark of aging, and cells are equipped with many systems to regulate mitochondrial structure and function in response to stress and metabolic alterations. Here, using budding yeast, we identify a proteolytic pathway that
Publikováno v:
eLife, Vol 3 (2014)
Replicative aging in yeast is asymmetric–mother cells age but their daughter cells are rejuvenated. Here we identify an asymmetry in pH between mother and daughter cells that underlies aging and rejuvenation. Cytosolic pH increases in aging mother
Externí odkaz:
https://doaj.org/article/97925d28da9a49f9a1821bca0d06b3fc
Publikováno v:
PLoS Genetics, Vol 7, Iss 3, p e1002015 (2011)
Somatic mutations contribute to the development of age-associated disease. In earlier work, we found that, at high frequency, aging Saccharomyces cerevisiae diploid cells produce daughters without mitochondrial DNA, leading to loss of respiration com
Externí odkaz:
https://doaj.org/article/b59cb071bda6446b82dd9eaa1cabfc9e
Autor:
Zara W. Nelson, Christina K. Leverich, Jessica J. Hsu, Matthew Fitzgibbon, Daniel E. Gottschling, Philip R. Gafken, Kiersten A. Henderson, Nathaniel H. Thayer
Publikováno v:
Proceedings of the National Academy of Sciences. 111:14019-14026
Long-lived proteins have been implicated in age-associated decline in metazoa, but they have only been identified in extracellular matrices or postmitotic cells. However, the aging process also occurs in dividing cells undergoing repeated asymmetric
Publikováno v:
Current Opinion in Cell Biology
Current opinion in cell biology, vol 26, iss 1
Current opinion in cell biology, vol 26, iss 1
Over 40 years ago, Francois Jacob proposed that levels of “integrons” explain how biological systems are constructed. Today, these networks of interactions between tissues, cells, organelles, metabolic pathways, genes, and individual molecules pr
Autor:
Thomas Nyström, Daniel E. Gottschling
Publikováno v:
Cell. 169(1)
Interconnectivity and feedback control are hallmarks of biological systems. This includes communication between organelles, which allows them to function and adapt to changing cellular environments. While the specific mechanisms for all communication
Publikováno v:
eLife
eLife, Vol 5 (2016)
eLife, Vol 5 (2016)
Mitochondrial dysfunction is a hallmark of aging, and underlies the development of many diseases. Cells maintain mitochondrial homeostasis through a number of pathways that remodel the mitochondrial proteome or alter mitochondrial content during time