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. 2012 Apr 24;2:379. doi: 10.1038/srep00379

Figure 4. 14-3-3γ plays a role in degrading oxidized proteins.

Figure 4

(a) 14-3-3γ does not affect the accumulation of Mieap and lysosomal proteins within mitochondria. The mitochondria were fractionated from the control and 14-3-3γ-KD A549 cells on day 3 after the IR. The mitochondrial fraction was subjected to a proteinase K protection assay. ProK: Proteinase K, (−): no treatment, (+): proteinase K treatment, Control: A549 control cells, 14-3-3γ-KD: A549 14-3-3γ-KD cells, Mitochondria: mitochondrial fraction, Cytosol: cytoplasmic fraction, Whole: whole cell lysate, Mieap α: endogenous Mieap α protein, and Mieap β: endogenous Mieap β protein. (b) 14-3-3γ deficiency causes the accumulation of oxidized proteins. The total cell lysates isolated from the control (1: cont), Mieap-KD (2: Mieap KD), and 14-3-3γ-KD (3: 14-3-3γ KD) A549 cells on day 3 after the IR. To evaluate the role of lysosomes, lysosome enzyme inhibitors were added to the A549 control cells on day 2 after the IR (4: cont/lysosome enzyme inhibitors). Then, the cell lysates were labeled by DNPH and subjected to Western blot analysis with anti-DNP antibody to detect the carbonyl-oxidized proteins. β-actin was used as a loading control. Full-length blots are presented in Supplementary Figure S8.