UHRF1 (Ubiquitin Like With PHD And Ring Finger Domains 1)

The conserved lysine residues K28, K29, and K41 on Tat were critical acceptor sites for ubiquitination and proteasomal degradation. Our findings revealed that YAP promotes the suppression of HIV-1 transcription and the maintenance of HIV-1 latency, providing novel insights into virus-host interactions for regulating HIV-1 latency.

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 senolytic Navitoclax targeted only a subset of senescent cells. Thus, the diversity of senescent cells driven by epigenetic changes can generate divergent outcomes. UHRF1 overexpression in zebrafish hepatocytes induces DNA damage leading to Atm-tp53-dependent senescence with UHRF1 levels dictating whether hepatocytes remain senescent, escape, or undergo senolytic elimination.

This study demonstrated that cholangiocarcinoma progression was suppressed by restoring miR-1 expression, suggesting that UHRF1 expression is involved in cholangiocarcinoma progression. The results of this study provide new insights into the molecular mechanisms underlying cholangiocarcinoma progression.

UHRF1 silencing restrained the malignant phenotype of melanoma cells by inhibiting the HOXA9/HIF-1α axis-mediated glycolysis, thus suppressing tumor growth in mice.

Furthermore, genetic disruption of the interaction between metformin and PRMT6 attenuates the inhibitory effect of metformin on breast cancer growth. Together, this work identifies a previously unrecognized mechanism for metformin to inhibit breast cancer growth.

MAZ promotes CRC cell migration, invasion, and EMT by transcriptionally activating UHRF1, which downregulates ECRG4 through DNA methylation.

Here, we report the development of H93, a hybrid small molecule integrating functional groups derived from NSC232003 and vorinostat, respectively...In vivo, H93 demonstrates significant antitumor efficacy. Overall, this study elucidates the structural and mechanistic basis of H93, establishing it as a promising UHRF1-targeted therapy for PCa.

Notably, experimental validation of PHF14 indicated its involvement in NPC malignancy, with downregulation of PHF14-suppressing cell migration, invasion, and proliferation. These discoveries give fresh perspectives on the molecular processes of NPC and offer potential biomarkers for clinical diagnosis and prognosis.

UHRF1 contributes to prostate cancer progression by driving tumor growth, metabolic reprogramming, and NF-κB activation. It holds promise as both a prognostic biomarker and a potential therapeutic target in PC.

This methylation pattern was associated with reduced survival rates and further validated its correlation with tumor metastasis in an independent cohort (n = 243). Our study elucidates that methylation-regulated alternative splicing contributes to phenotypic heterogeneity in GC, highlighting its potential advantage over differentially expressed genes in improving stratification strategies for precision oncology.

At the molecular level, USP11 interacted with UHRF1 and maintained its stabilization by removing ubiquitin. Sevo could protect LPS-induced HMC3 cell apoptosis, inflammation, and oxidative stress by regulating the USP11/UHRF1 axis, which might provide a novel therapeutic mechanism for Sevo in SCI.