factor (GEF) for Rab21 and an effector for Rab32 and Rab38, and binds to VPS29, targeting it to endosomes (Hesketh et al., 2014). In addition, the Rab GTPase-activating protein (GAP) TBC1D5 also requires the retromer CSC for its membrane association, and interestingly, binds to VPS29 via the same hydrophobic surface patch as VARP does (Harbour et al., 2010; Hesketh et al., 2014). Overexpression of TBC1D5 causes the retromer CSC to be displaced from the membrane in a similar manner to the expression of the GDP-locked (and therefore inactive) T22N mutant of Rab7a and thus it has been suggested that TBC1D5 could function as a GAP for Rab7a where the retromer CSC is localised (Seaman et al., 2009).
