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. 2019 Aug 9;33(11):11735–11745. doi: 10.1096/fj.201900766R

Figure 3.

Figure 3

Accumulation of ubiquitinated proteins and autophagy adaptors occur early in ULK2-deficient muscles. Data were obtained from control and ULK-deficient TA muscles 1 wk after electroporation. A) Representative immunoblots of LC3 (LC3A/B), adaptor proteins, and ubiquitinated proteins in control and ULK2-deficient muscles of mice with normal food access or after 24 h of starvation. B) Quantification of LC3, adaptor proteins, and ubiquitinated proteins (n = 5–8). C) mRNA levels of genes encoding Lc3a and Lc3b (Map1lc3a and Map1lcb, respectively), adaptor proteins p62 (Sqstm1) and Nbr1, and ubiquitin [ubiquitin b (Ubb) and unibquitin c (Ubc)] in control and ULK2-deficient muscles of mice with normal food access (left) and after 24-h starvation (right) (n = 5). D) Representative immunoblots of LC3 (LC3A/B), adaptor proteins, and ubiquitinated proteins in control and ULK1-deficient muscles of mice with normal food access or after 24 h of starvation. E) Quantification of LC3, adaptor proteins, and ubiquitinated proteins (n = 6–8). F) mRNA levels of the genes indicated in C in control and ULK1-deficient muscles of mice with normal food access (left) and after 24 h of starvation (right) (n = 4). UB, ubiquitin. Data are means ± sem. *P < 0.05.