TRIM31 (Tripartite Motif Containing 31)

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.

NLRP3 neddylation hinders its interaction with Trim31 and thereby inhibits its K48-linked ubiquitination and subsequent degradation. MLN4924, a potent compound NAE inhibitor in phase 1/2/3 clinical trials for cancers, alleviates psychological stress-induced NLRP3 inflammasome activation, microglia inflammatory activation, and anxiety-like behavior, suggesting novel clinical activity of MLN4924.

On the other hand, it also activated iron-sulfur cluster assembly 2 (ISCA2)-mediated iron-sulfur cluster (ISC) assembly and iron starvation response to inhibit cuproptosis and ferroptosis. Collectively, our findings indicated the mechanism of the synergistic effect of ferroptosis and cuproptosis in the treatment of GC and presented a prospective therapeutic strategy through elucidating the molecular mechanism of ferroptosis and cuproptosis mediated by MTF1.

In both in vitro and in vivo models, TRIM31 promoted the proliferation, migration, and invasion of GC cells. Given its frequent overexpression in various malignancies, TRIM31 could represent a valuable indicator of poor prognosis and altered immune infiltration in individuals with cancer.

Our findings provide new evidence that TRIM31 may promote cell proliferation and that Snai2 may impair Wnt/β-catenin signaling pathway activity through the transcriptional inhibition of TRIM31. These findings provide new ideas for the regulation of tumor growth and targeted therapy by Snai2-TRIM31 and the Wnt/β-catenin pathway axis.

Furthermore, TRIM31 facilitates the entry of P65 into the nucleus, which in turn creates a positive feedback pathway that promotes inflammatory-carcinogenic transformation and tumorigenesis of colorectal. Our findings indicate that TRIM31 may be an important factor driving colorectal carcinogenesis, providing a potential target for intervention in CRC targeted therapy.

TRIM31 enhances the proliferation, migration, and invasion of Eca109 cells through the ubiquitination of BBOX1. In conclusion, TRIM31 functions as an oncogene, suggesting its potential as a novel therapeutic target or prognostic biomarker for patients with esophageal cancer.

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.

In this study, the expression and distribution of MHCRDEGs in STAD were analyzed by various methods, and a clinical prediction model of STAD was constructed using MHCRDEGs. The validity of this model confirms the feasibility of MHCRDEGs as prognostic markers for STAD, elucidating their potential clinical implications in guiding treatment strategies for this disease.

Sorafenib and lenvatinib are frontline treatments for advanced hepatocellular carcinoma (HCC). TRIM29 degrades YBX1 through ubiquitination, thereby inhibiting the PI3K/AKT signaling pathway and reversing lenvatinib resistance in HCC. TRIM29 can serve as an independent prognostic indicator of survival and recurrence in HCC patients, and it may provide new avenues for developing innovative treatment strategies for HCC.

IL-17 induces PD-L1 gene transcription in NSCLC cells through TRIM31-dependent MEF2C K63-linked polyubiquitination.

SOCS2 contributes to the suppression of type 1 interferon signaling, aiding viral persistence, while TRIM31 promotes the degradation of the tumor suppressor protein TSC, activating the mTORC1 pathway and potentially promoting liver cell proliferation. These findings suggest that FGF21 upregulation in HCV-infected cells may play a role in both immune response regulation and cell proliferation, contributing to sustained viral infection and disease progression.