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. 2018 Nov 26;316(2):H392–H399. doi: 10.1152/ajpheart.00714.2018

Fig. 6.

Fig. 6.

The Bcl-2-associated athanogene 3 (Bag3) P209L knockin (KI) mutation does not impair stress-inducible heat shock protein (HSP) expression, ubiquitination, or autophagy in the heart. A and B: representative immunoblots (A) and corresponding quantitative densitometric analysis (B) of HSP70, heat shock cognate (HSC)70, and HSP90. The blots shown were derived from replicate samples run on parallel gels as described in Fig. 5A. C and D: representative immunoblots (C) and corresponding quantitative densitometric analysis (D) of ubiquitin (Ub). EG: representative immunoblots (E) and corresponding quantitative densitometric analysis (F and G) of cardiac autophagy markers in wild-type (+/+) control and heterozygous (m/+) and homozygous (m/m) Bag3 P209L KI mutant mouse hearts at 16 mo of age after 18 h of starvation. GAPDH or Ponceau staining served as a loading control. The blots shown were derived from replicate samples run on parallel gels as described in Fig. 5A. Data were normalized to corresponding GAPDH levels or Ponceau staining, and mutant groups are expressed as fold changes versus control. n = 3 for each group. Data are presented as means ± SE.