UBD (Ubiquitin D)

Concurrently, chromatin immunoprecipitation and luciferase reporter assays demonstrate that the Spi-B transcription factor (SPIB) directly interacts with the UBD promoter, leading to the activation of its transcription. Collectively, these findings identify the SPIB/UBD/MMP3 axis as a pivotal regulator of TNBC metastasis, indicating its value for prognostic evaluation and targeted therapy.

Our data suggest that active TGF-β1/SMAD signaling contributes to the loss of KLF4 expression in human HCC through FAT10-mediated ubiquitin-independent proteasomal degradation and direct transcriptional suppression.

In conclusion, UBD is a key gene associated with disease severity and T cells infiltration in cholestasis. These findings provide new insight into the key biomarker of cholestasis and further highlight that UBD might be a promising novel therapeutic target for patients with cholestasis.

Drug sensitivity profiling nominated imatinib (Vina score: -8.9 kcal/mol) and TTNPB as potential therapies for UBD-high tumors, validated by stable MD simulations. In esophageal carcinoma (ESCA), UBD expression escalated with tumor stage and predicted poor survival (p<0.05).UBD enhances the proliferation and migration of esophageal cancer cells by modulating the TP53 signaling pathway, as validated through transcriptomic analysis and functional assays. This study advances UBD as a prognostic indicator and therapeutic target, bridging molecular insights with clinical translation in precision oncology.

This study uncovers a new neuropathology underlying T1DM-associated DN: Bcl-XL activation associates PERK and ubiquitination marker upregulation in sensory neurons. Bcl-XL inactivation in nociceptors might be a potential target for relieving neuropathic pain of T1DM.

Olaparib treatment in xenograft mice overexpressing UBD significantly reduced tumor growth (p < 0.05), inhibited Gln metabolism pathways, and enhanced HCC cell autophagy. Olaparib targeted UBD to promote autophagy in HCC by inhibiting Gln metabolism pathways.

UBD plays an oncogenic role in HCC by encouraging proliferation and EMT through promoting CTNNA3 degradation. These findings suggest that targeting the UBD/CTNNA3 axis could be a potential therapeutic strategy for HCC management.

Pathway analysis implicated UBD in neurodegeneration, proteolysis, and apoptosis. Collectively, our study demonstrates that UBD is a promising prognostic biomarker and a potential predictor of immunotherapy sensitivity in multiple cancer types.

The results indicate that UBD promotes M2 macrophage polarization through glycolytic reprogramming, enhancing immune evasion and ITR in OC. Inhibiting UBD or targeting glycolytic pathways may provide new strategies for improving OC immunotherapy.

To address this limitation, compound 12 was synthesized with an ethyl hydrazide ZBG, significantly improving oral bioavailability (53 %). These findings highlight compound 12 as a promising lead for further pharmacophore optimization, paving the way for clinically viable HDAC6 selective inhibitors with enhanced drug-like properties.

Based on TF regulatory networks in the tumor microenvironment, this study developed a 9-gene risk model for the prognosis of ovarian cancer. This model may aid in the future promotion of personalized OC immunotherapy. In addition, JCHAIN, UBD, and RARRES1 were identified as three novel immune-related biomarkers for OC.

GSEA showed that the expression of UBD involved with various pathways including epithelial-mesenchymal transition (EMT), PI3K-AKT-mTOR signaling, P53 pathway, angiogenesis, inflammatory response, KRAS signaling, hypoxia, as well as TGF-β signaling. Furthermore, our findings suggest that UBD accelerates the activation of EMT and PI3K/AKT/mTOR pathway.