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. 1997 Oct 6;139(1):49–61. doi: 10.1083/jcb.139.1.49

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Model for the ARF6-regulated PM–endosomal recycling pathway. We propose that activation of ARF6, through nucleotide exchange, occurs at the tubular endosome and triggers the recycling of membrane to discrete sites at the PM where ARF6-GTP stimulates the formation of protrusive structures, rich in actin. Inactivation, through GTP hydrolysis, signals the return of ARF6 to the tubular endosome via membrane intermediates that are yet to be defined. CD treatment or expression of the GTP-binding–defective mutant of ARF6, T27N, blocks recycling out to the PM. In contrast, AlF treatment or expression of the GTPase-defective mutant, Q67L, blocks membrane internalization back into the tubular endosomal compartment.