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. 2012 May 28;197(5):659–675. doi: 10.1083/jcb.201111079

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© 2012 Longatti et al.

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Figure 10. — Model for role of TBC1D14 and Rab11 mediating vesicular transport from the RE to the expanding phagophore. Under fed conditions, Rab11-positive REs function in recycling to the plasma membrane. Upon amino acid starvation, Rab11 mediates vesicle formation from the RE directed to forming autophagosomes. This process is negatively regulated by TBC1D14, which functions as an effector for Rab11. TBC1D14 dissociates from Rab11-positive REs in starvation and accumulates on the Golgi complex. Overexpression of TBC1D14 causes tubulation of REs, accumulation of the ULK1 complex and Rab11 on REs, and inhibition of vesicular transport from the RE.