TRIM proteins in autophagy: selective sensors in cell damage and innate immune responses

被引:144
作者
Di Rienzo, Martina [1 ]
Romagnoli, Alessandra [1 ]
Antonioli, Manuela [1 ]
Piacentini, Mauro [1 ,2 ]
Fimia, Gian Maria [1 ,3 ]
机构
[1] Natl Inst Infect Dis L Spallanzani IRCCS, Dept Epidemiol Preclin Res & Adv Diagnost, Rome, Italy
[2] Univ Roma Tor Vergata, Dept Biol, Rome, Italy
[3] Sapienza Univ Rome, Dept Mol Med, Rome, Italy
关键词
FAMILY PROTEINS; DEGRADATION; ULK1; MECHANISMS; TARGETS; INFLAMMATION; CONTRIBUTES; RESTRICTION; RECOGNITION; SUMOYLATION;
D O I
10.1038/s41418-020-0495-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autophagy, a main intracellular catabolic process, is induced in response to a variety of cellular stresses to promptly degrade harmful agents and to coordinate the activity of prosurvival and prodeath processes in order to determine the fate of the injured cells. While the main components of the autophagy machinery are well characterized, the molecular mechanisms that confer selectivity to this process both in terms of stress detection and cargo engulfment have only been partly elucidated. Here, we discuss the emerging role played by the E3 ubiquitin ligases of the TRIM family in regulating autophagy in physiological and pathological conditions, such as inflammation, infection, tumorigenesis, and muscle atrophy. TRIM proteins employ different strategies to regulate the activity of the core autophagy machinery, acting either as scaffold proteins or via ubiquitin-mediated mechanisms. Moreover, they confer high selectivity to the autophagy-mediated degradation as described for the innate immune response, where TRIM proteins mediate both the engulfment of pathogens within autophagosomes and modulate the immune response by controlling the stability of signaling regulators. Importantly, the elucidation of the molecular mechanisms underlying the regulation of autophagy by TRIMs is providing important insights into how selective types of autophagy are altered under pathological conditions, as recently shown in cancer and muscular dystrophy.
引用
收藏
页码:887 / 902
页数:16
相关论文
共 121 条
[1]   cGAS in action: Expanding roles in immunity and inflammation [J].
Ablasser, Andrea ;
Chen, Zhijian J. .
SCIENCE, 2019, 363 (6431) :1055-+
[2]  
[Anonymous], 2019, J MOL BIOL
[3]  
[Anonymous], 2019, J MOL BIOL
[4]  
[Anonymous], CELL DEATH DIFFER
[5]   Emerging Mechanisms in Initiating and Terminating Autophagy [J].
Antonioli, Manuela ;
Di Rienzo, Martina ;
Piacentini, Mauro ;
Fimia, Gian Maria .
TRENDS IN BIOCHEMICAL SCIENCES, 2017, 42 (01) :28-41
[6]   AMBRA1 Interplay with Cullin E3 Ubiquitin Ligases Regulates Autophagy Dynamics [J].
Antonioli, Manuela ;
Albiero, Federica ;
Nazio, Francesca ;
Vescovo, Tiziana ;
Perdomo, Ariel Basulto ;
Corazzari, Marco ;
Marsella, Claudia ;
Piselli, Pierluca ;
Gretzmeier, Christine ;
Dengjel, Joern ;
Cecconi, Francesco ;
Piacentini, Mauro ;
Fimia, Gian Maria .
DEVELOPMENTAL CELL, 2014, 31 (06) :734-746
[7]   A KRAB/KAP1-miRNA Cascade Regulates Erythropoiesis Through Stage-Specific Control of Mitophagy [J].
Barde, Isabelle ;
Rauwel, Benjamin ;
Marin-Florez, Ray Marcel ;
Corsinotti, Andrea ;
Laurenti, Elisa ;
Verp, Sonia ;
Offner, Sandra ;
Marquis, Julien ;
Kapopoulou, Adamandia ;
Vanicek, Jiri ;
Trono, Didier .
SCIENCE, 2013, 340 (6130) :350-353
[8]   Origin and Evolution of TRIM Proteins: New Insights from the Complete TRIM Repertoire of Zebrafish and Pufferfish [J].
Boudinot, Pierre ;
van der Aa, Lieke M. ;
Jouneau, Luc ;
Du Pasquier, Louis ;
Pontarotti, Pierre ;
Briolat, Valerie ;
Benmansour, Abdenour ;
Levraud, Jean-Pierre .
PLOS ONE, 2011, 6 (07)
[9]   TRIMming down to TRIM37: Relevance to Inflammation, Cardiovascular Disorders, and Cancer in MULIBREY Nanism [J].
Brigant, Benjamin ;
Metzinger-Le Meuth, Valerie ;
Rochette, Jacques ;
Metzinger, Laurent .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2019, 20 (01)
[10]   Inflammasomes: mechanism of assembly, regulation and signalling [J].
Broz, Petr ;
Dixit, Vishva M. .
NATURE REVIEWS IMMUNOLOGY, 2016, 16 (07) :407-420