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Chapter 12 Monitoring Autophagic Degradation of p62/SQSTM1

Bjørkøy, Geir, Lamark, Trond, Pankiv, Serhiy, Øvervatn, Aud, Brech, Andreas, Johansen, Terje·2009·Methods in Enzymology
DOI 10.1016/s0076-6879(08)03612-4
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Abstract

The p62 protein, also called sequestosome 1 (SQSTM1), is a ubiquitin-binding scaffold protein that colocalizes with ubiquitinated protein aggregates in many neurodegenerative diseases and proteinopathies of the liver. The protein is able to polymerize via an N-terminal PB1 domain and can interact with ubiquitinated proteins via the C-terminal UBA domain. Also, p62/SQSTM1 binds directly to LC3 and GABARAP family proteins via a specific sequence motif. The protein is itself degraded by autophagy and may serve to link ubiquitinated proteins to the autophagic machinery to enable their degradation in the lysosome. Since p62 accumulates when autophagy is inhibited, and decreased levels can be observed when autophagy is induced, p62 may be used as a marker to study autophagic flux. Here, we present several protocols for monitoring autophagy-mediated degradation of p62 using Western blots, pulse-chase measurement of p62 half-life, immunofluorescence and immuno-electron microscopy, as well as live cell imaging with a pH-sensitive mCherry-GFP double tag. We also present data on species-specificity and map the epitopes recognized by several commercially available anti-p62 antibodies.

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Crossref · 10.1016/s0076-6879(08)03612-4

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  • SQSTM1 can modulate the NFE2L2/NRF2 anti-oxidant response pathway through a KEAP1 binding domain.

    “In the context of autophagy as a stress response, the complexity of using SQSTM1 as an autophagy marker protein is underscored by its capacity to modulate the NFE2L2/NRF2 anti-oxidant response pathway through a KEAP1 binding domain [592,593].”

    From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [592]

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Research works printed but not linked: 20

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  2. Gal, 2007, p62 accumulates and enhances aggregate formation in model systems of familial amyotrophic lateral sclerosis, J. Biol. Chem., 282, 11068, 10.1074/jbc.M608787200 · DOI
  3. Hara, 2008, FIP200, a ULK‐interacting protein, is required for autophagosome formation in mammalian cells, J. Cell Biol., 181, 497, 10.1083/jcb.200712064 · DOI · Paper page
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Metadata

Authors
Bjørkøy, G., Lamark, T., Pankiv, S., Øvervatn, A., Brech, A., & Johansen, T.
Venue
Methods in Enzymology
Publisher
Elsevier
Published
2009
Pages
181-197
ISSN
0076-6879
DOI
10.1016/s0076-6879(08)03612-4
Cited by
1,069
References
8
Language
en

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