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. 2013 May 3;288(25):18366–18380. doi: 10.1074/jbc.M113.469882

FIGURE 2.

FIGURE 2.

The ERAD of CFTR and CPY* is Lhs1-independent, and the nucleotide exchange factor Sil1 is dispensable for αENaC degradation. A and B, cycloheximide chase reactions were performed as described under “Experimental Procedures” in LHS1 wild-type (filled circles) or Δlhs1 (open circles) yeast strains expressing a C-terminally 3HA epitope-tagged form of CFTR or a C-terminally 3HA-tagged form of CPY*. C, cycloheximide chase reactions were performed as described above in SIL1 (filled circles) or Δsil1 (open circles) yeast strains expressing a C-terminally HA epitope tagged form of αENaC. All chase reactions were performed at 37 °C, and lysates were immunoblotted with anti-HA antisera (ENaC, CFTR, and CPY*) and with anti-G6P as a loading control. Data represent the means of 4–7 experiments, ±S.E.