Monitoring autophagic degradation of p62/SQSTM1.
By G. Bjørkøy, T. Lamark, S. Pankiv, Aud Øvervatn, A. Brech, T. Johansen. Methods in Enzymology, 2009
1,117 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6497619fd27db4b9757f8545e8b71368efb29da5
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In Cell Biology
- D. Klionsky
- I. Slaninová
- Beth Levine
- V. Deretic
- Yongqiang Chen
- Eric H. Baehrecke
- R. Shaw
- Guillermo Mariño
In Epidemiology
- D. Klionsky
- Beth Levine
- I. Slaninová
- N. Mizushima
- Guido Kroemer
- V. Deretic
- Alec C. Kimmelman
- D. Rubinsztein
In Molecular Biology
- Beth Levine
- D. Klionsky
- I. Slaninová
- Alec C. Kimmelman
- Guido Kroemer
- V. Deretic
- Eric H. Baehrecke
- Guillermo Mariño
Citations in the corpus
- Inhibition of mTOR by Rapamycin Abolishes Cognitive Deficits and Reduces Amyloid-β Levels in a Mouse Model of Alzheimer's Disease (2010, background): “To determine whether the decreased LC3-II/bactin ratios in hippocampi of rapamycin-treated PDAPP mice resulted from the induction of autophagic flux, we examined LC3 distribution, as well as levels of p62SQSTM, an ubiquitin-binding scaffold protein that is specifically degraded by autophagy[22,45], ”
- The dynamic nature of autophagy in cancer. (2011, background): “p62/SQSTM1 has multiple critical functions and is ultimately degraded by autophagy, so serially monitoring levels of p62 may also be considered a relative measure of flux (Bjorkoy et al. 2009).”
- Pancreatic cancers require autophagy for tumor growth. (2011, positive): “To confirm that we were inhibiting autophagy in tumors, we measured p62 expression, a scaffold protein known to be degraded by autophagy (Bjorkoy et al. 2009).”
- TFEB-mediated autophagy rescues midbrain dopamine neurons from α-synuclein toxicity (2013, background): “Western blot analysis showed that failure of the ALP was associated with a progressive accumulation of α-syn oligomers that was previously shown to be toxic for nigral neurons (44) and the autophagy substrate p62 (16, 45) (Fig.”
- Autophagy: assays and artifacts (2010, background): “For example, changes in p62 (SQSTM1/sequestosome 1) protein levels are used to indicate a defect in the turnover of poly-ubiquitinated protein aggregates [21].”
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (2012, positive): “Yet another solution is to employ a radioactive pulse-chase assay to measure the rates of SQSTM1 degradation.(425)”
- Guidelines for the use and interpretation of assays for monitoring autophagy (2012, methodology): “Yet another solution is to employ a radioactive pulse-chase assay to measure the reates of p62 degradation.(330) Western blot analysis using NP40 or Triton X-100 lysis in autophagic conditions typically shows a reduction in p62 levels.”
- Macrophage Autophagy Plays a Protective Role in Advanced Atherosclerosis (2012, background): “…p62/SQSTM1, which is known to accumulate when autophagy flux through lysosomes is defective, i.e., through decreased p62 lysosomal degradation (Bjorkoy et al., 2009) (Figure 3B). p62 immunofluorescence was present in 10%–15% of intimal cells in macrophage-rich areas of lesions of 8 week…”
- The eIF2α/ATF4 pathway is essential for stress-induced autophagy gene expression (2013, background): “As p62 was shown to be itself a selective autophagy substrate continuously degraded by autophagy (41,42) with a 2-h half-life under amino acid starvation (52), we would expect the p62 protein level to be decreased during leucine starvation.”