TRIP13 (Thyroid Hormone Receptor Interactor 13)

P2, N=50, Not yet recruiting, Universiteit Antwerpen

Using this cell line, we showed that splicing to the HPV16 E2 3'-splice site SA2709 could be perturbed by over expression of SR-proteins or by incubation with a pan-Akt kinase inhibitor. These proteins and substances shifted splicing from E2 splice site SA2709 to the upstream HPV16 3'-splice site SA2582 and enhanced nLuc production, thereby demonstrating the utility of the pE1nLuc cell line as a bioassay for HPV16 E2 mRNA splicing.

We also established a subcutaneous transplantation tumor model in NB NOD/scid mice, and sh-LINC01296 or sh-TRIP13 inhibited tumor growth in mice, and the tumor growth in the sh-LINC01296 + OE-TRIP13 group and the sh-TRIP13 + OE-LINC01296 group was between the NC group and the sh-LINC01296 or sh-TRIP13 group. These results suggest that LINC01296 may play a role as an oncogene in the development of tumorigenesis in NB by mediating TRIP13, and provide a marker for the prognosis of NB.

Ultimately, understanding the genetic regulation of DSB repair pathways can provide critical insights into genome stability maintenance and reveal new therapeutic opportunities in cancer. Future work should focus on pathway crosstalk, phase-specific regulation, and integrating repair modulation into personalized medicine.

The development of ccRCC is significantly influenced by MRGs, particularly TRIP13. This study can assist in offering ccRCC patients individualized treatment options.

These findings uncover a previously unrecognized role of TRIP13 in regulating mitochondrial integrity under proteotoxic stress, thereby contributing to BTZ resistance. Targeting TRIP13 may represent a novel therapeutic approach to improve outcomes in MM patients.

Interestingly, TRIP13 reciprocally regulates the stability of the CSE1L protein, indicating a bidirectional regulatory loop. The CSE1L-TRIP13 axis provides a robust theoretical foundation to develop targeted therapeutic strategies, offering novel insights into the clinical treatment of GC patients.

Among MLWH, HPV16 E6 antibodies are strongly associated with OPSCC, yet point estimates of the sensitivity and specificity of HPV16 E6 antibodies for OPSCC were lower compared to studies in populations without HIV.

We further found that the melatonin receptor 1B (MTNR1B), rather than melatonin receptor 1 A (MTNR1A), is essential for MT mediated TRIP13 downregulation. Because we also found that treatment with MT still decreases cell proliferation of TRIP13-KO cells, combining MT with the TRIP13 inhibitor DCZ0415 would likely have an additive anti-proliferative therapeutic effect in the treatment of NSCLC.

This study establishes a visceral pain model centered on pancreatic parenchymal nociception rather than secondary neural effects, and for the first time proposes an interconnected regulatory network linking epigenetic modifications, immune reprogramming, and neural plasticity, revealing dual pain pathogenesis mechanisms: (1) immune microenvironment reshaping that potentiates neuroinflammation, and (2) direct ion channel regulation enhancing neuronal excitability. These findings provide a mechanistic foundation for developing methylation-based prognostic biomarkers and multimodal analgesic therapeutic strategies targeting the immuno-neural nexus.

Immune cell infiltration analysis demonstrated that TRIP13 expression is negatively correlated with the infiltration of CD4+ T cells, CD8+ T cells, and B cells. TRIP13 emerges as a candidate independent prognostic indicator and a promising intervention point for GC treatment.

We functionally established important roles of epithelial-derived TRIP13 and SUMOylation, and cancer-associated fibroblast-derived SULF1 and BGN in HGSC progression. These findings provide unique molecular insights into HGSC pathogenesis and identify potential new therapeutic targets for intervention.