The role of autophagy during the early neonatal starvation period
By Akiko Kuma, M. Hatano, M. Matsui, A. Yamamoto, H. Nakaya, T. Yoshimori, Y. Ohsumi, T. Tokuhisa, N. Mizushima. Nature, 2004
3,017 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/c710a105eda480b665bec4b09a6af2acdcde5e55
How researchers see this paper
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In Epidemiology
- N. Mizushima
- Beth Levine
- Guido Kroemer
- D. Klionsky
- I. Slaninová
- E. White
- Alec C. Kimmelman
- V. Deretic
In Molecular Biology
- Guido Kroemer
- Beth Levine
- N. Mizushima
- E. White
- D. Klionsky
- David M. Sabatini
- Alec C. Kimmelman
- I. Slaninová
In Surgery
- Beth Levine
- N. Mizushima
- David M. Sabatini
- Guido Kroemer
- Ralph J. Deberardinis
- Craig B. Thompson
- R. Kaufman
- D. Klionsky
Citations in the corpus
- Autophagy regulates programmed cell death during the plant innate immune response. (2005, background): “In mammals, autophagy regulates survival during neonatal starvation, embryonic development, and tumorogenesis (Kuma et al., 2004; Liang et al., 1999; Qu et al., 2003; Yue et al., 2003).”
- Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress (2010, background): “For example, mice lacking Atg5 , which is required for autophagosome formation, are born at mendelian ratios, but die within 1 day of delivery because they are unable to mobilize the energy and nutrient stores they require to survive the pre-suckling period (Kuma et al., 2004).”
- Autophagy: Renovation of Cells and Tissues (2011, background): “Similarly, mice with systemic deletion of Atg3 (Sou et al., 2008), Atg5 (Kuma et al., 2004), and Atg7 (Komatsu et al., 2005) die immediately after birth and show reduced amino acid levels in tissues and plasma during the neonatal starvation period.”
- Fission and selective fusion govern mitochondrial segregation and elimination by autophagy (2008, methodology): “ATG5þ /þ and ATG5 / mouse embryonic fibroblasts (MEFs) transfected with pEF321-T, and an SV40 large T antigen expression vector were a generous gift from N Mizushima and were previously described (Kuma et al, 2004).”
- Cytosolic FoxO1 is essential for the induction of autophagy and tumour suppressor activity (2010, background): “In response to such diverse stimuli as genotoxic chemicals, oxidative reagents and serum starvation, autophagy is induced for the maintenance of cellular metabolism or for the elimination of harmful damaged proteins and organelles, thus facilitating cell surviva”
- The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress (2007, background): “The principal role of autophagy is to supply nutrients for surviva”
- Lysosomes and autophagy in cell death control (2005, background): “For example, mice lacking Atg5 survive without any major developmental defect until birth, but succumb to the stressful neonatal period unless newborns are force-fed milk in the first hours after birt”
- Autophagy is important in islet homeostasis and compensatory increase of beta cell mass in response to high-fat diet. (2008, background): “The principal role of autophagy is to reallocate nutrients from unnecessary processes to more pivotal processes required for survival (Kuma et al., 2004).”
- Cardiac autophagy is a maladaptive response to hemodynamic stress. (2007, background): “The increase in autophagosome-localized GFP-LC3 in stressed cardiac myocytes indicates autophagosome accumulation (14, 20).”