Molecular switches of SQSTM1: the impact of post-translational modifications on autophagy and neurodegeneration
What this study shows
Comprehensive review of how post-translational modifications (phosphorylation, ubiquitination, acetylation, S-acylation, S-nitrosylation) tune SQSTM1/p62's role as the autophagy cargo-receptor hub -- relevant to neurodegenerative disease (Alzheimer's, ALS, Huntington's) where SQSTM1 regulation goes awry.
At a glance
| Evidence type | R Review — secondary literature, not a new result Marked R because it is a review or synthesis of existing evidence rather than a new primary result; that is a different form of writing, not a weaker one. |
| Study type | Narrative Review |
| Model system | Review |
| Journal | Autophagy |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1080/15548627.2026.2711593 · PMID 42560011 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | none (review) |
| Target | SQSTM1/p62 / MTORC1 / autophagy |
| Model | Review |
| Effect | Summarises how PTMs of SQSTM1 tune its autophagy-receptor function and its regulation of and by MTORC1. |
In the Atlas
Related topics
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- Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule (2024)
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