TABLE 5.

Relationship between TRIMs and autophagy.

Name	Target	Mechanism	Effect	References
TRIM16	Lysosomal membrane permeation	TRIM 16 and Galectin-3 synergistically recognize LMP, induce lysosomal selective autophagy, and mediate lysosomal damage	Lysosome dysfunction and hemolysis impairment associated with accelerated cell senescence	Araya et al. (2021)
TRIM21	Fc receptor	TRIM21 signaling is inhibited by its B-box domain and activated by phosphorylation. B-box occupies E2 binding sites in the catalytic ring domain by simulating E2-E3 interactions, inhibiting TRIM21 ubiquitination and preventing immune activation.	The intracellular antibody signal is regulated, and B-box is a key regulator of RING E3 ligase activity	Niida et al. (2010), Dickson et al. (2018)
TRIM39	Rab7	TRIM39 interacts with Rab7 and promotes Rab7 activity by inhibiting its ubiquitination at lysine 191 residues. Knockdown TRIM39 also inhibits autophagy degradation of p53	Inhibition of colorectal cancer progression and autophagy flux	Hu et al. (2021)
TRIM63	p62	Interacts with P62 to regulate the conversion of nicotine to acetylcholine receptors	Increased the turnover of muscle-type CHRN in a TRIM63-dependent manner, enhanced production of endo/lysosomal carriers of CHRN	Khan et al. (2014)
TRIM13	p62/SQSTM1	TRIM13 was stable during ER stress, interacting with P62 /SQSTM1 and co-locating with DFCP1.	Regulate the initiation of autophagy and decrease the clonogenesis ability of cells during ER stress	Tomar et al. (2012)
TRIM23	TBK1	Ubiquitination of TRIM23 via K27 linkage depends on GTPase to activate TBK1	Virus-induced autophagy is mediated by activation of TBK1	Sparrer et al. (2017)
TRIM41	EI24	EI24 targets RING E3 ligase, is involved in transcription, proteolysis, cell bioenergetics, and apoptosis, and is regulated by TP53 and MTOR signaling	EI24 participates in UPS autophagy crosstalk through RING E3 ligase degradation