Publication: TRIMs and Galectins Globally Cooperate and TRIM16 and Galectin-3 Co-direct Autophagy in Endomembrane Damage Homeostasis
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Issued Date
2016-10-10
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ISSN
18781551
15345807
15345807
Other identifier(s)
2-s2.0-84992645517
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Mahidol University
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SCOPUS
Bibliographic Citation
Developmental Cell. Vol.39, No.1 (2016), 13-27
Suggested Citation
Santosh Chauhan, Suresh Kumar, Ashish Jain, Marisa Ponpuak, Michal H. Mudd, Tomonori Kimura, Seong Won Choi, Ryan Peters, Michael Mandell, Jack Ansgar Bruun, Terje Johansen, Vojo Deretic TRIMs and Galectins Globally Cooperate and TRIM16 and Galectin-3 Co-direct Autophagy in Endomembrane Damage Homeostasis. Developmental Cell. Vol.39, No.1 (2016), 13-27. doi:10.1016/j.devcel.2016.08.003 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/42895
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Title
TRIMs and Galectins Globally Cooperate and TRIM16 and Galectin-3 Co-direct Autophagy in Endomembrane Damage Homeostasis
Abstract
© 2016 Elsevier Inc. Selective autophagy performs an array of tasks to maintain intracellular homeostasis, sterility, and organellar and cellular functionality. The fidelity of these processes depends on precise target recognition and limited activation of the autophagy apparatus in a localized fashion. Here we describe cooperation in such processes between the TRIM family and Galectin family of proteins. TRIMs, which are E3 ubiquitin ligases, displayed propensity to associate with Galectins. One specific TRIM, TRIM16, interacted with Galectin-3 in a ULK1-dependent manner. TRIM16, through integration of Galectin- and ubiquitin-based processes, coordinated recognition of membrane damage with mobilization of the core autophagy regulators ATG16L1, ULK1, and Beclin 1 in response to damaged endomembranes. TRIM16 affected mTOR, interacted with TFEB, and influenced TFEB's nuclear translocation. The cooperation between TRIM16 and Galectin-3 in targeting and activation of selective autophagy protects cells from lysosomal damage and Mycobacterium tuberculosis invasion.