Asymmetric Inheritance of Oxidatively Damaged Proteins During Cytokinesis

By H. Aguilaniu, L. Gustafsson, M. Rigoulet, T. Nyström. Science, 2003

661 citations recorded by the source corpus.

Subfields: Geriatrics and Gerontology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/615feb0f004654a2e7df46078c4111a76a80db7f

How researchers see this paper

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

In Geriatrics and Gerontology

1. D. Sinclair
2. R. Mostoslavsky
3. S. Millard
4. S. Wood
5. Toren Finkel
6. T. Nyström
7. Jie Liu
8. F. Alt

In Molecular Biology

1. S. Millard
2. S. Wood
3. R. Mostoslavsky
4. G. Jayaraj
5. C. L. Klaips
6. D. Sinclair
7. F. Hartl
8. T. Nyström

In Physiology

1. S. Millard
2. S. Wood
3. R. Mostoslavsky
4. D. Sinclair
5. F. Hartl
6. T. Nyström
7. I. Dalle-Donne
8. A. Milzani

Citations in the corpus

• Pathways of cellular proteostasis in aging and disease (2018, background): “This is thought to be due to at least in part an increase in the accumulation of errors in translation, splicing, or molecular misreading and to an increased production of oxidized and carbonylated proteins (Aguilaniu et al., 2003; López-Otín et al., 2013).”
• SIRTUIN 1 AND SIRTUIN 3: PHYSIOLOGICAL MODULATORS OF METABOLISM (2012, background): “Sir2 is also required to segregate damaged proteins into the mother cell, thus sparing the daughter cell (4).”
• Riding the DUBway: regulation of protein trafficking by deubiquitylating enzymes (2006, positive): “Even in yeast, senescence accompanies the accumulation of oxidatively modifi ed proteins, more than half of which are cytosolic (with the remainder being mitochondrial; Aguilaniu et al., 2003).”
• Protein carbonylation, cellular dysfunction, and disease progression (2006, background): “Interestingly, carbonylated proteins accumulating with replicative age are not inherited by daughter cells during cytokinesis [31].”
• Replicative and Chronological Aging in Saccharomyces cerevisiae (2012, neutral): “, 2004a, 2005), and other factors (Alvers et al., 2009; Fabrizio et al., 2010; Goldberg et al., 2009).”
• Cellular strategies for controlling protein aggregation (2010, background): “Protein aggregates, and particularly carbonylated proteins, have been suggested as such possible senescence factor”
• A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy (2008, background): “Although to our knowledge there have been no genetic studies in yeast demonstrating a role for yeast Sir2 in autophagy, it is of interest to note that in Saccharomyces cerevisiae, Sir2 has been shown to be required for the proper segregation of damaged proteins between mother and daughter cells (27)”
• Trends in oxidative aging theories. (2007, background): “Considering the high rates of flux through glycolysis in yeast, ensuing production of reactive aldehydes such as methyglyoxal (leaked from triosephosphate isomerase [57,58]) and the clonal aging-related increase in protein carbonyls [43], we suggest that advanced glycation end products [59,60] may p”
• Role of oxidative carbonylation in protein quality control and senescence (2005, background): “Moreover, actin staining indicates that sir2 mutants are somewhat defective in actin filament organization during cytokinesis (Aguilaniu et al, 2003).”