the small Ras-like GTPase Sar1 (Sar1 H79G) [36]. This constitutively active mutant of Sar1 prevents un-coating of transport vesicles, blocking ER export by inhibiting recycling of COPII components [37]. In OK cells expressing mutant Sar1 H79G, CNIH-2 was retained in the ER, while in neighboring non-transfected cells expressing endogenous wildtype Sar1, the accumulation of CNIH-2 in the Golgi remained unchanged (Fig. 3A). Thus, CNIH-2 is selectively exported from the ER in a COPII-dependent manner.
