Phosphorylation of OPTN by TBK1 enhances its binding to Ub chains and promotes selective autophagy of damaged mitochondria
By Benjamin Richter, Danielle A. Sliter, Lina Herhaus, Alexandra Stolz, Chunxin Wang, Petra Beli, Gabriele Zaffagnini, P. Wild, S. Martens, Sebastian A. Wagner and 2 more. Proceedings of the National Academy of Sciences of the United States of America, 2016
682 citations recorded by the source corpus.
Subfields: Epidemiology, Neurology
View Paper: https://www.semanticscholar.org/paper/048a2810bfdcb3f573b04d48e3cdc03a7e203795
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In Epidemiology
- Fiona M Menzies
- D. Rubinsztein
- Angeleen Fleming
- V. Deretic
- Koji Yamano
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In Neurology
- Fiona M Menzies
- Koji Yamano
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- Miyuki Sato
- Mashun Onishi
- Koji Okamoto
- D. Rubinsztein
- B. Padman
Citations in the corpus
- Molecular mechanisms and physiological functions of mitophagy (2021, positive): “TBK1 kinase in PINK1/Parkin-mediated mitophagy During PINK1/Parkin-mediated mitophagy, TBK1 directly or indirectly mediates phosphorylation of all known autophagy receptors (Richter et al , 2016).”
- Autophagy and Neurodegeneration: Pathogenic Mechanisms and Therapeutic Opportunities. (2017, positive): “Disease-associated mutations in this kinase have been shown to reduce binding of TBK1 to OPTN and thus decrease the clearance of dysfunctional mitochondria (Richter et al., 2016).”
- The mitophagy pathway and its implications in human diseases (2023, background): “63,64 A pathogenic E478G mutation in UBAN domain makes OPTN less able to bind to ubiquitin, thereby inhibiting mitophagy.”
- Autophagy in inflammation, infection, and immunometabolism (2021, background): “In addition to type I IFN activation, TBK1 is important for autophagy (Kumar et al., 2019; Pilli et al., 2012; Ravenhill et al., 2019; Richter et al., 2016; Vargas et al., 2019; Wild et al., 2011; Zachari et al., 2019) (Figure 2E,F).”
- Deciphering the Molecular Signals of PINK1/Parkin Mitophagy. (2016, background): “Recent work has shown that Optineurin is phosphorylated by TRAF-associated NFkB activator (TANK)-binding kinase 1 (TBK1) during mitophagy and this enhances its binding to ubiquitin chains (discussed below) [44,47].”
- Atg8 family LC3/GABARAP proteins are crucial for autophagosome–lysosome fusion but not autophagosome formation during PINK1/Parkin mitophagy and starvation (2016, background): “The primary PINK1/ Parkin mitophagy receptors, optineurin and NDP52 (Wong and Holzbaur, 2014; Lazarou et al., 2015), function by promoting ULK1 recruitment to damaged mitochondria to initiate autophagosome biogenesis (Lazarou et al., 2015).”