TRIM5 (Tripartite Motif Containing 5)

Moreover, it correlates with immune infiltration and may be relevant to immunotherapy in these cancers. Furthermore, its correlation with tumor protein 53 (TP53), alpha/beta hydrolase domain containing 5 (ABHD5), and evolutionarily conserved signaling intermediate in toll pathway (ECSIT) may be used as a potential area of therapeutic intervention.

Eugenol can effectively overcome osimertinib resistance in NSCLC by regulating glycolysis through the TRIM59/ERK signaling pathway. Eugenol could serve as a promising adjunctive therapy to improve chemotherapy efficacy and overcome drug resistance in NSCLC.

Our integrative approach highlights the potential of genomic and immune microenvironment data in developing personalized risk models for BCa, offering insights into individualized treatment strategies. Importantly, TRIM59 is involved in ferroptosis resistance in BCa. These findings have potential implications for identifying diagnostic biomarkers and therapeutic targets for BCa treatment.

These findings underscore the potent anti-metastatic and anti-angiogenic effects of NK-1R antagonism in glioblastoma and highlight aprepitant as a promising candidate for future in vivo and in ovo therapeutic investigations targeting extracellular matrix (ECM) remodeling, chemotaxis, and angiogenesis.

Mechanistically, TRIM59 knockdown is associated with heightened activation of TLR4/JNK-p38/NF-κB signaling pathways to promote inflammation, increase adipogenesis and lipogenesis related genes while decreased lipolysis and β-oxidation related genes expression to increase lipid accumulation, simultaneously increased Bax and caspase 3 while decreased Bcl-2 expression to induce apoptosis, thereby leading to obesity. Taken together, our findings define a new critical biological role of TRIM59 in the regulation of diet-induced obesity through attenuating inflammation, improving lipid metabolism and apoptosis, and we conclude that TRIM59 may provide a novel insight in therapeutic target research for treatment of obesity-associated metabolic diseases.

TRIM56 promotes pancreatic cancer progression through activation of the TRAF6/NF-κB signaling pathway. Targeting TRIM56 represents a promising therapeutic strategy for pancreatic cancer treatment.

In particular, the apoptosis rate was significantly increased in the TRIM5-siRNA2 or TNFSF10-siRNA2 and C1QBP-siRNA2 group compared to the only C1QBP-siRNA2 group. These findings provide a deeper understanding of the role of C1QBP in apoptosis and could pave the way for further study investigating the role and mechanism of C1QBP protein in mediating the regulation of cell apoptosis by ORFV.

Using optogenetics, we demonstrate that the E3 activity of TRIM37 is directly coupled to the assembly state of its substrates, being activated only when centrosomal proteins cluster into higher-order assemblies resembling MTOCs. This regulatory framework provides a mechanistic basis for understanding TRIM37-driven pathologies and echoes the restriction of the human immunodeficiency virus capsid by TRIM5, thus unveiling a conserved activation blueprint among TRIM proteins to control turnover of complexes assembled at the mesoscale level.

TRIM59 conferred gemcitabine resistance in PC by promoting RBPJ K63-linked ubiquitination, followed by activating Notch signaling. Therefore, our study provides a promising target for gemcitabine sensitization in PC treatment.

Furthermore, TRIM55 attenuated the association between NF90 and the mRNA of HIF1α and TGF-β2, consequently reducing their stability and inactivating the HIF1α/VEGF and TGFβ/Smad signaling pathways. In conclusion, our findings unveil the important roles of TRIM55 in suppressing the progression of HCC partly by promoting the degradation of NF90 and subsequently modulating its downstream pathways, including HIF1α/VEGF and TGFβ/Smad signaling.

Moreover, patients with a high RS may be better candidates for nonimmune therapy due to lower half-maximal inhibitory concentration values of drugs (such as AKT inhibitors and gemcitabine)...This helped to better find patients with these characteristics and suitable treatments using this method. Collectively, the findings of the present study indicate that PSS combined with RS has great potential to evaluate the prognosis of patients with virus -related HCC and assist in deciding treatment strategies.

Using optogenetics, we demonstrate that TRIM37's E3 activity is directly coupled to the assembly state of its substrates, activating only when centrosomal proteins cluster into higher-order assemblies resembling MTOCs. This regulatory framework provides a mechanistic basis for understanding TRIM37-driven pathologies and, by echoing TRIM5's restriction of the HIV capsid, unveils a conserved activation blueprint among TRIM proteins for controlling mesoscale assembly turnover.