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Autophagy receptors

Unless otherwise stated all data on this page refer to the human proteins. Gene information is provided for human (Hs), mouse (Mm) and rat (Rn).


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Autophagy receptors are important for protein homeostasis, by regulating the clearance of protein aggregates, pathogens and the turnover of a wide range of cargo proteins, via the autophagosome-lysosome pathway, by ubiquitin-dependent and -independent mechanisms [3]. Their activity is modulated by protein modifications such as phosphorylation and ubiquitination. Some autophagy receptors have been associated with neurodegenerative diseases [2,10].


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sequestosome 1 Show summary »

Target Id 3213
Nomenclature sequestosome 1
Previous and unofficial names autophagy receptor p62 | p62
Genes SQSTM1 (Hs), Sqstm1 (Mm), Sqstm1 (Rn)
Ensembl ID ENSG00000161011 (Hs), ENSMUSG00000015837 (Mm), ENSRNOG00000003147 (Rn)
UniProtKB AC Q13501 (Hs), Q64337 (Mm)
YTK-2205 (Activation) [4]
Comment Sequestosome 1 (widely referred to as p62) is the most studied 'selective' autophagy receptor. It facilitates autophagy of certain protein aggregates (aggrephagy), pathogens (xenophagy) and enzymes (zymophagy). Kinases that phosphorylate sequestosome 1 include ULK1 [5], TBK1 [8],CK2 [6] and p38δ. It is ubiquitinated by the E3 ubiquitin transferase TRIM21 [2,7]. These protein modifications regulate sequestosome 1's activity and selectivity for cargo proteins. Genetic variants in SQSTM1 are associated with amyotrophic lateral sclerosis (ALS; NMD)/frontotemporal lobar degeneration (FTLD) [9,11] and Alzheimer's disease [1].


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How to cite this family page

Database page citation:

Autophagy receptors. Accessed on 25/02/2024. IUPHAR/BPS Guide to PHARMACOLOGY,

Concise Guide to PHARMACOLOGY citation:

Alexander SPH, Kelly E, Mathie AA, Peters JA, Veale EL, Armstrong JF, Buneman OP, Faccenda E, Harding SD, Spedding M, Cidlowski JA, Fabbro D, Davenport AP, Striessnig J, Davies JA et al. (2023) The Concise Guide to PHARMACOLOGY 2023/24: Introduction and Other Protein Targets. Br J Pharmacol. 180 Suppl 2:S1-22.