TRIM3 (Tripartite Motif Containing 3)

The results are in line with previous observations of segregation errors in human cell lines with TRIM37 defects. Further studies are required to elucidate the prevalence and implications of mosaic aneuploidies in Mulibrey nanism.

In summary, this study revealed, for the first time, that lutein alleviates PD progression by increasing Drp1 ubiquitination and degradation via TRIM31 transcription and translation, ultimately improving neuronal mitochondrial function. These findings not only elucidate a novel mechanism underlying lutein's neuroprotective effect but also identify a potential therapeutic target and offer a new strategy for PD treatment.

Sustained IFN-β secretion subsequently inhibits NSCLC cell proliferation and reprograms the tumor microenvironment by increasing the infiltration levels of CD4+ T cells, M1 macrophages and NK cells. Our findings revealed a reciprocal negative feedback loop in the regulation of IFN-β signaling, highlighting the role of the TRIM3/TLR3 axis in the suppression of NSCLC progression and offering a promising strategy to suppress tumor growth and enhance immunotherapy efficacy in NSCLC.

Here, cyclophilin A (CypA) is identified as a critical mediator of cisplatin (DDP)/paclitaxel (DTX) resistance in NSCLC by suppressing ferroptosis, an iron-dependent form of regulated cell death...knockout of CypA or pharmacological inhibition with cyclosporine A (CsA) reverse resistant NSCLC cells to DDP/DTX both in vitro and in vivo by restoring ferroptosis...The study uncovers a CypA/SLC7A11/TRIM3 axis governing ferroptosis evasion in NSCLC chemoresistance and highlights CypA as a promising therapeutic target. Repurposing CsA to inhibit CypA represents a translatable strategy to overcome chemotherapy resistance, offering preclinical validation for improving outcomes in NSCLC patients.

In vivo experiments further confirmed that RNF220 aggravated tumor growth and metastasis. In summary, these findings indicate that RNF220 promotes HCC progression by regulating USP22 and activating the Akt pathway, suggesting that RNF220 may serve as a potential biomarker and therapeutic target for HCC.

Then, we demonstrated that TRIM3 directly interacted with YAP1, and TRIM3 reduced YAP1 stability by inducing ubiquitination modification. Finally, rescue assays showed that si-YAP1 treatment alleviated the effects of si-TRIM3 on melanoma cells.This study indicated that depletion of TRIM3 strengthened the proliferation and mobility of M14 and A375 cells, suppressed cell apoptosis, but these phenomena were counteracted by YAP1 down-regulation.

Oligomerization resulting from RING-RING interactions and conformational regulation through B-box 2-B-box 2 interfaces are essential for TRIM37 to suppress centrobin condensate formation. These results indicate that, similar to antiviral TRIM ligases, TRIM37 activation is coupled to detection of oligomerized substrates, facilitated by recognition of specific motifs in the substrate, to enforce ubiquitination-mediated clearance of ectopic centrosomal protein assemblies.

In a recent work, we found that Drosophila p53 controls asymmetric stem cell division (ASCD) in neural stem cells by transcriptionally activating core ASCD regulators, such as the conserved cell-fate determinants Numb and Brat (NUMB and TRIM3/TRIM2/TRIM32 in humans, respectively). In this short communication, we comment on this new finding, the mild phenotypes associated with Drosophila p53 mutants in this context, as well as novel avenues for future research.

In conclusion, ubiquitin ligases emerge as key regulators of NLRP3 inflammasome activation, exhibiting a complex array of functions that finely tune immune responses. Understanding these regulatory mechanisms not only sheds light on fundamental aspects of inflammation but also offers potential therapeutic avenues for inflammatory disorders and infectious diseases.

Through the establishment of cisplatin (cDDP)-resistant CESC cell lines, we discovered that the expression of TRIM3 was further downregulated in cDDP-resistant cells, while overexpression of TRIM3 enhanced cellular sensitivity to cDDP...Consequently, overexpressing TRIM3 in drug-resistant cells facilitates PERK activation and subsequent induction of apoptosis through inhibition of GRP78, ultimately suppressing drug resistance and inducing apoptosis in CESC cells. In conclution, our study suggests that the TRIM3/GRP78 axis regulates cDDP resistance in CESC cells by modulating the downstream apoptotic pathway of ERS.

Further studies have shown that the K351 site of P53 is the key site mediating the ubiquitination of P53 K48-linked to promote aerobic glycolysis in ESCC and tumor cell growth. Our results reveal that the TRIM33-P53 signal axis regulates glycolysis during ESCC and may provide a new perspective for the diagnosis and treatment of ESCC.

Administration of YU102 in the DSS-treated colitis model mice caused suppression of the NLRP3 protein levels and accompanied inflammatory cytokine release in the intestinal epithelium. Taken together, we demonstrated that inhibiting IP under inflammatory conditions induces E3 ligase TRIM31-mediated NLRP3 degradation, leading to attenuation of the NLRP3 inflammatory response that triggers disruption of intestinal barrier.