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. Author manuscript; available in PMC: 2010 Jun 12.
Published in final edited form as: Cell. 2009 Jun 12;137(6):1062–1075. doi: 10.1016/j.cell.2009.03.048

Figure 1. Elevated and persistent p62 in autophagy-defective tumor cells under metabolic stress.

Figure 1

(A) Domain organization of p62 illustrating the Phox and Bem1p (PB1) oligomerization domain (p62 and atypical Protein Kinase C [aPKC]), the Zinc finger (ZZ) Rip 1 binding domain, the TRAF6 binding site (TBS), the microtubule associated protein light chain 3 (LC3) domain (LC3/ATG8 binding), and the ubiquitin-associated (UBA) (poly-ubiquitin binding).

(B) IF of endogenous p62 showing accumulation and persistence of p62 in autophagy-defective cells under normal growth conditions (Day 0), 7 days of metabolic stress (Day 7I), and 1 (Day 7+1R) and 2 (Day 7+1R) days of recovery.

(C) Autophagy-defective cells express constitutively higher levels of exogenous Myc-p62. Six independent cell lines of Bcl-2-expressing atg5+/+ and atg5−/− iBMK cells stably expressing Myc-tagged p62 were evaluated for p62 expression levels by Western blotting with an antibody to Myc tag.