<scp>ULK</scp>
            1 translocates to mitochondria and phosphorylates
            <scp>FUNDC</scp>
            1 to regulate mitophagy

Wu, Wenxian; Tian, Weili; Hu, Zhe; Guo, Chen; Huang, Lei; Wen, Li; Zhang, Xingli; Xue, Peng; Zhou, Changqian; Liu, Lei; Zhu, Yushan; Zhang, Xingliang; Li, Longxuan; Zhang, Liangqing; Sui, Sen‐Fang; Zhao, Bin; Feng, Du

doi:10.1002/embr.201438501

Cited by 452 publications

(401 citation statements)

References 38 publications

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“…These receptors mediate the engulfment of targeted mitochondria by autophagosome for lysis [125][126][127]. Other Parkin/ PINK1-independent pathways can mediate mitophagy alternatively involving NIX/BNIP3, Ambra1, ULK1 or cardiolipin in neurons [128][129][130][131][132]. Interestingly, among the Parkin targets are Mfn-1-2 and Miro1.…”

Section: Mitochondrial Dynamics and Mitophagy In Cancermentioning

confidence: 99%

The mitochondrial dynamics in cancer and immune-surveillance

Simula

Nazio

Campello

2017

Seminars in Cancer Biology

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A B S T R A C TMitochondria-shaping proteins control the dynamic equilibrium between fusion and fission of the mitochondrial network. Their balance is strictly required to regulate various processes, including the quality of mitochondria, cell metabolism, cell death, proliferation and cell migration. Alterations in these processes are frequently encountered in cancer, during both its onset and later progression, as evidence emerge connecting alterations in mitochondrial dynamics with cancer development. In recent years, novel therapeutic approaches to fight against different human tumors aim at exploiting the immune system's ability to specifically recognize tumor antigens, thus killing malignant cells in a process named immune-surveillance. Interestingly, data are accumulating on the role that mitochondrial dynamics play also for the correct function of both the innate and the adaptive immune system. By this review, we overview how mitochondrial dynamics can affect various processes during cancer development, acting directly on tumor cells or indirectly on cells responsible for tumor aggression and defence.

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Section: Mitochondrial Dynamics and Mitophagy In Cancermentioning

confidence: 99%

The mitochondrial dynamics in cancer and immune-surveillance

Simula

Nazio

Campello

2017

Seminars in Cancer Biology

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“…Bcl2-L1/ Bcl-XL binding to PGAM5 inhibits its phosphatase activity, preventing FUNDC1-mediated mitophagy (Wu et al, 2014a). ULK1, as the other major regulator, was shown to be recruited to fragmented mitochondria under hypoxia and to phosphorylate Ser17 of FUNDC1, enhancing the binding to LC3 (Wu et al, 2014b). Although these phosphorylation sites are just a few residues apart, their impact on the interaction of the protein to LC3 is remarkable and the structural basis of this interaction was intensively studied (Lv et al, 2017).…”

Section: Fundc1mentioning

confidence: 99%

How to get rid of mitochondria: crosstalk and regulation of multiple mitophagy pathways

Zimmermann

Reichert

2017

Biological Chemistry

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Mitochondria are indispensable cellular organelles providing ATP and numerous other essential metabolites to ensure cell survival. Reactive oxygen species (ROS), which are formed as side reactions during oxidative phosphorylation or by external agents, induce molecular damage in mitochondrial proteins, lipids/ membranes and DNA. To cope with this and other sorts of organellar stress, a multi-level quality control system exists to maintain cellular homeostasis. One critical level of mitochondrial quality control is the removal of damaged mitochondria by mitophagy. This process utilizes parts of the general autophagy machinery, e.g. for the formation of autophagosomes but also employs mitophagy-specific factors. Depending on the proteins utilized mitophagy is divided into receptor-mediated and ubiquitin-mediated mitophagy. So far, at least seven receptor proteins are known to be required for mitophagy under different experimental conditions. In contrast to receptor-mediated pathways, the Pink-Parkin-dependent pathway is currently the best characterized ubiquitin-mediated pathway. Recently two additional ubiquitin-mediated pathways with distinctive similarities and differences were unraveled. We will summarize the current state of knowledge about these multiple pathways, explain their mechanism, and describe the regulation and crosstalk between these pathways. Finally, we will review recent evidence for the evolutionary conservation of ubiquitin-mediated mitophagy pathways.

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“…The phosphorylation of Ser17 enhances FUNDC1 binding to LC3, inducing mitophagy [79]. MicroRNA-137 (miR-137), which is mainly expressed in the brain and regulates neural stem cell determination [80], is hypoxia-responsive microRNAs that targets two mitophagic receptors, NIX and FUNDC1, and significantly inhibits hypoxia-induced mitophagy [81].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%