Seminars in Immunopathology

, Volume 32, Issue 4, pp 431–436

Selective degradation of p62 by autophagy

Review

DOI: 10.1007/s00281-010-0220-1

Cite this article as:
Ichimura, Y. & Komatsu, M. Semin Immunopathol (2010) 32: 431. doi:10.1007/s00281-010-0220-1

Abstract

The autophagy–lysosome pathway is a highly conserved bulk degradation system in eukaryotes. During starvation, cytoplasmic constituents are non-selectively degraded by autophagy, and the resulting amino acids are utilized for cell survival. By taking advantage of mouse genetics, many physiological functions of mammalian autophagy have been uncovered. Growing lines of evidences have revealed the essential role of constitutive (or basal) autophagy in cellular homeostasis through its selectivity. p62, one of the selective substrates for autophagy, plays a key role in the formation of cytoplasmic proteinaceous inclusion, a hallmark of conformational diseases such as Alzheimer’s disease, Parkinson’s disease, and various chronic liver disorders. In this review, we discuss the physiological roles of the selective turnover of p62 by autophagy and their molecular mechanisms.

Keywords

AutophagySelective autophagyp62

Abbreviations

Ape1

Aminopeptidase I

Atg

Autophagy-related

DISC

Death-inducing signaling complex

LC3

Microtubule-associated protein 1 light chain 3

LIR

LC3-interacting region

LRS

LC3 recognition sequence

PB1

Phox and Bem1p

PE

Phosphatidylethanolamine

UBA

Ubiquitin-associated domain

UPS

Ubiquitin–proteasome system

Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  1. 1.Protein Metabolism ProjectTokyo Metropolitan Institute of Medical ScienceSetagaya-kuJapan