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. 2012 Jul 31;287(39):33014–33025. doi: 10.1074/jbc.M112.389148

FIGURE 2.

FIGURE 2.

CNK3 positively regulates ENaC surface expression and activity. A, knockdown of endogenous CNK3 decreases ENaC activity in mpkCCDc14 cells. mpkCCDc14 cells stably expressing CNK3 or control (non-target) shRNA were plated on Transwell filters and allowed to grow to high resistance. The cell monolayers were then treated with aldosterone (1 μm for 3 h) prior to determination of ENaC activity. Shown is the -fold change in aldosterone-induced equivalent short circuit current in CNK3 shRNA-expressing cells. Also shown is a representative blot demonstrating knockdown of endogenous CNK3. ***, p < 0.001 compared with control (n = 6). B, cell surface biotinylation assay for ENaC in HEK 293T cells transiently transfected with FLAG-tagged α-, β-, and γ-mENaC subunits. After transfection, cells were treated with EZ-Link sulfo-NHS-biotin before protein extraction and recovered by affinity immobilization using NeutrAvidin-conjugated agarose beads followed by immunoblot (IB) analysis with anti-β-ENaC antibody. Shown is a graphical representation of CNK3-dependent augmentation of surface ENaC based on multiple repeats of biotinylation assays. Also shown is a representative blot demonstrating CNK3 overexpression. ***, p < 0.001 compared with control (n = 4). Error bars represent S.E. WCL, whole-cell lysate.