Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice.

By M. Komatsu, S. Waguri, Masato Koike, Yu-shin Sou, T. Ueno, Taichi Hara, N. Mizushima, Jun-ichi Iwata, J. Ezaki, S. Murata and 15 more. Cell, 2007

2,205 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f893f203f04c7c42022dcb8042525d9b44763eed

How researchers see this paper

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

In Cell Biology

1. D. Klionsky
2. I. Slaninová
3. N. Mizushima
4. Beth Levine
5. E. White
6. Guido Kroemer
7. Alec C. Kimmelman
8. V. Deretic

In Epidemiology

1. Beth Levine
2. N. Mizushima
3. D. Klionsky
4. I. Slaninová
5. Guido Kroemer
6. Alec C. Kimmelman
7. E. White
8. V. Deretic

In Molecular Biology

1. Guido Kroemer
2. Beth Levine
3. N. Mizushima
4. D. Klionsky
5. I. Slaninová
6. Douglas R. Green
7. E. White
8. Alec C. Kimmelman

Citations in the corpus

• Autophagy in malignant transformation and cancer progression (2015, positive): “Reactive oxygen species (ROS) are highly genotoxic, and autophagy prevents their overproduction by removing dysfunctional mitochondria (Green et al , 2011; Takahashi et al , 2013) as well as redox-active aggregates of ubiquitinated proteins (Komatsu et al , 2007; Mathew et al , 2009).”
• Persistent activation of Nrf2 through p62 in hepatocellular carcinoma cells (2011, methodology): “The Atg7f/f;Alb-Cre mice described previously by our group (Komatsu et al., 2007) were used in this study.”
• A periodic diet that mimics fasting promotes multi-system regeneration, enhanced cognitive performance and healthspan (2015, background): “Autophagy can bemonitored by indirectly measuring autophagic sequestration (LC3) and degradation (p62) (Moscat and Diaz-Meco, 2011) (Figure S1Y and S1Z). p62 is consistently increased in autophagy-deficient cells (Komatsu et al., 2007).”
• Nix is a selective autophagy receptor for mitochondrial clearance (2010, background): “Receptor proteins, p62 and neighbour of BRCA1 gene 1 (NBR1), which interact with both ubiquitin (Ub) and autophagosome-specific Ub-like (UBL) proteins, Atg8-family proteins LC3/GABARAP, have been identified”
• Molecular mechanisms of the Keap1–Nrf2 pathway in stress response and cancer evolution (2011, background): “Targeted deletion of Atg7 in liver results in the accumulation of p62 as inclusion bodies in hepatocytes and leads to liver injury (Komatsu et al. 2007).”
• Eaten alive: a history of macroautophagy (2010, background): “One possible autophagy receptor is p62/SQSTM1, a multifunctional adaptor protein that contains an LC3-interacting region (LIR) and a ubiquitin-associated (UBA) domai”
• p62 links the autophagy pathway and the ubiqutin–proteasome system upon ubiquitinated protein degradation (2016, neutral): “autophagy-null mice, but not in autophagy-normal mice [11].”
• p62 links autophagy and Nrf2 signaling. (2015, background): “In this study, p62 was found to mediate the formation of protein aggregates destined for autophagic turnover, which suggested that p62 facilitated selective degradation of protein cargo via autophagy [26].”
• Autophagy: Renovation of Cells and Tissues (2011, background): “Simultaneous deletion of either p62 or Nrf2 dramatically attenuates the liver injury resulting from autophagy deficiency (Komatsu et al., 2007a, 2010).”
• Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages. (2014, background): “Whereas p62 is normally degraded by the autophagolysosome, it accumulates under conditions of failed autophagy (Komatsu et al., 2007).”
• Autophagy gone awry in neurodegenerative diseases (2010, neutral): “These other functions of p62 could explain in part why deletion of p62 ameliorates hepatic injury in animals deficient for macroautophagy in live”
• The mitophagy pathway and its implications in human diseases (2023, background): “Accumulation of P62-enriched ubiquitin-positive aggregates was found in cells with defective autophagy due to ATG7 deficiency, and genetic ablation of P62 reduced ubiquitin-positive aggregates.(44,45) P62 is primarily degraded in lysosomes via autophagy, indicating that it functions as an autophagy ”
• Serine 403 phosphorylation of p62/SQSTM1 regulates selective autophagic clearance of ubiquitinated proteins. (2011, background): “The atg5-deficient mice showed ubiquitin-positive inclusions in Molecular Cell 44, 27 neurons (Hara et al., 2006), and these inclusions were p62 positive as also reported in atg7-deficient mice (Komatsu et al., 2007).”