Author: Cadwell, Ken; Debnath, Jayanta
Title: Beyond self-eating: The control of nonautophagic functions and signaling pathways by autophagy-related proteins Document date: 2018_3_5
ID: s1qd3x1b_23_1
Snippet: et al., 2016) . Deletion of ATG9L1, but not other ATGs, increases the colocalization between STI NG and TBK-1 to enhance IFN-I production in response to cytosolic DNA ( Fig. 3 ; Saitoh et al., 2009) . Also, generation of cGAMP by cGAS activates ULK1, which phosphorylates and inhibits STI NG while also inducing autophagy ( Fig. 3 ; Konno et al., 2013) . Similarly, Beclin-1 can bind and inhibit cGAS and simultaneously mediate the degradation of cyt.....
Document: et al., 2016) . Deletion of ATG9L1, but not other ATGs, increases the colocalization between STI NG and TBK-1 to enhance IFN-I production in response to cytosolic DNA ( Fig. 3 ; Saitoh et al., 2009) . Also, generation of cGAMP by cGAS activates ULK1, which phosphorylates and inhibits STI NG while also inducing autophagy ( Fig. 3 ; Konno et al., 2013) . Similarly, Beclin-1 can bind and inhibit cGAS and simultaneously mediate the degradation of cytoplasmic DNA through autophagy ( Fig. 3 ; Liang et al., 2014) . Thus, Beclin-1 prevents sustained cGAS activation through both direct inhibition and depriving the enzyme of its substrate. In these examples, conserved autophagy proteins (ATG9L1, ULK1, and Beclin-1) display functions independent of autophagy-related processes, although these functions do not necessarily preclude their role in classic autophagy.
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