Figure 6
From: Expression of truncated Kir6.2 promotes insertion of functionally inverted ATP-sensitive K+ channels
Schematic representation of protein orientation. Immunocytochemical and electrophysiological data support a model where Kir6.2ΔC26, which lacks native ER retention and membrane trafficking signals, is abnormally inserted in the plasma membrane (left), suggesting abnormal trafficking. Conversely, inclusion of a large, water-soluble domain on the N-terminus imparts a sufficient energy barrier such that all the proteins are inserted in a unidirectional manner, overcoming the lack of ER retention and trafficking signals (right).
