PSMD12 (Proteasome 26S Subunit, Non-ATPase 12)

Cycloheximide chase and MG132 assays confirmed that PSMD12 stabilized CDK1 by inhibiting proteasome-mediated degradation...PSMD12 promoted LUAD progression by modulating CDK1 ubiquitination and enhancing cell cycle progression. These findings suggest that PSMD12 is a promising molecular target for future LUAD therapies.

A novel three-gene prognostic model for CRC was developed and validated, offering therapeutic insights through molecular networks and drug predictions.

Mechanistically, PSMD12 interacts with cyclin-dependent kinase 1 (CDK1), preventing its degradation through deubiquitination, thereby accelerating HCC progression by enhancing cell cycle progression. These findings underscore PSMD12's role in HCC and highlight its potential as both a prognostic biomarker and therapeutic target, providing new insights into the molecular mechanisms driving HCC progression.

PSMD12 emerges as a crucial gene in promoting BM, potentially serving as an early warning indicator of BM in early-stage LUAD. The upstream regulatory network of PSMD12 overexpression provides potential mechanisms for BM in LUAD patients.

Together with a complete literature review, we expanded the clinical spectrum of STISS, highlighting the relevance of inherited variants, and discussing challenges in diagnosis and management. We finally consider the intriguing role of PSMD12 in human development and propose to index "onychoheterotopia" among the Human Phenotype Ontology terms.

PSMD12 promotes NSCLC progression by activating the Nrf2/TrxR1 pathway, providing a novel prognostic and therapeutic target for NSCLC treatment.

This work reveals the essential roles of PSMD12 in the proliferation and apoptosis of PC development. PSMD12 may regulate CDKN3 expression by interacting with and abating the ubiquitination level of CDKN3, thereby participating in the malignant behavior of PC.

All these accessions corresponded to a window of the proteins modulated in response to the bystander effect. Our chondrosarcoma model clarified the nature of the bystander response of chondrocytes and may suggest several interesting new mechanisms that are specific to particular irradiation doses and qualities.

The xenograft models supported the results of cell experiments. In conclusion, PSMD12 could activated MEK-ERK pathway via KIF15 upregulation, thereby promoting tumor progression.

These results indicate that H9c2 and HepG2 cells are sensitive to prometryn in-vitro. However, prometryn effects on the heart and liver tissue in male mice is significantly different. Overall, our data supports the deduction that prometryn affected mitochondrial function, induced oxidative stress in cells, but also alters the ubiquitin-proteasome system and increases oxidative stress in mice liver. These results help towards elucidation of the mechanism by which prometryn could cause diseases.

PSMD2 has been shown to be an independent predictor for OS in BLCA patients based on univariate and multivariate analysis (P < .001). Overall, according to this study, PSMD2 and PSMD8 could be served as a prognostic biomarker for BLCA patients.

The expression of hsa-miR-181d, hsa-miR-185, hsa-miR-15b, hsa-miR-214 and hsa-miR-496 was significantly different between normal tissue and EAC. CDH1, GART, GTSE1, NEK2 and hsa-miR-496, hsa-miR-214, hsa-miR-15b were found to be correlated with survival.