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. 2016 Oct 21;9(5):399–408. doi: 10.1080/21541248.2016.1240495

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© 2016 The Author(s). Published with license by Taylor & Francis

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 2. — C9orf72 regulates the Rab1a dependent trafficking of the ULK1 complex. Upon inhibition of mTOR, the inhibitory phosphorylation of ULK1 is lost, leading to the activation of ULK1. Active ULK1 phosphorylates the other members of the initiation complex, including FIP200 and ATG13. Functioning as a Rab1a effector, C9orf72 mediates the interaction between the active ULK1 initiation complex and GTP-Rab1a within its target membrane. Thus C9orf72 controls the Rab1a dependent trafficking of the ULK1 initiation complex to the phagophore. How Rab1 is activated in response to autophagy induction is not yet known.