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Fig. 2. Residue 822 of the putative CNBD is crucial for trafficking of HERG. (A) Cells expressing HERG_wt, HERG_V822M and HERG_V822P mutants were treated with dimethylsulfoxide (control) or proteasomal inhibitors (lactacystin, ALLN, MG132) 1 day after transfection. Cells were lysed and equal amounts of the soluble fraction were separated on SDS-PAGE and subjected to immunoblotting with an anti-HA antibody. (B) Live cells expressing the mutant channel were treated with proteinase K (PK) (+) or untreated (–). PK was blocked with extensive washes and equal amounts of detergent soluble fraction was subjected to immunoblot analysis for HA and CASK (left) and N-cadherin (N-Cad) (right). The arrow (Deg) indicates the product generated by the PK. Quantifications were performed by measuring pixel intensity of the HA and the N-Cad signals before and after PK treatment and normalized to the corresponding CASK signal. (C) Patch clamp analysis of cells co-transfected with CD8 cDNA along with HERG_wt and the HERG_V822M mutant. Mock transfections were performed with CD8 cDNA. Depolarization steps were imposed on cells decorated with beads.

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