A5074314695- Protein Degradation and Inhibitors
- Histone Deacetylase Inhibitors Research
- Multiple Myeloma Research and Treatments
- Epigenetics and DNA Methylation
- Viral Infectious Diseases and Gene Expression in Insects
- 3D Printing in Biomedical Research
- Surfactants and Colloidal Systems
- Genomics, phytochemicals, and oxidative stress
- Nanoparticle-Based Drug Delivery
- Cancer-related gene regulation
- Peroxisome Proliferator-Activated Receptors
- Protein Interaction Studies and Fluorescence Analysis
- Pluripotent Stem Cells Research
- Virus-based gene therapy research
- CRISPR and Genetic Engineering
- Electrospun Nanofibers in Biomedical Applications
- Endoplasmic Reticulum Stress and Disease
- Genomics and Chromatin Dynamics
- RNA Research and Splicing
- Redox biology and oxidative stress
- Glutathione Transferases and Polymorphisms
- RNA modifications and cancer
Wuhan University
2021-2024
University of California, San Diego
2023
Jinan University
2018-2019
Clear cell renal carcinoma (ccRCC) is characterized by glycogen-laden, unexplained male predominance, and frequent mutations in the Von Hippel-Lindau (
Aggresomes are the product of misfolded protein aggregation, and presence aggresomes has been correlated with poor prognosis in cancer patients. However, exact role tumorigenesis progression remains largely unknown. Herein, multiomics screening reveal that OTUD1 plays an important retaining ovarian stem cell (OCSC) properties. Mechanistically, elevated levels lead to formation OTUD1-based cytoplasmic aggresomes, which is mediated by a short peptide located intrinsically disordered N-terminal...
Cell-loaded carboxymethylcellulose (CMC) microspheres were generated via a flow focusing microfluidic device, with final aim to obtain viable ATDC5 aggregates sustained proliferation capacity. We synthesized various CMC phenolic groups (CMC-Ph) and demonstrated that high CMC-Ph molecular weight, concentration (>0.8 g/ml) or long culturing period had obvious inhibition effect on proliferation, but low horseradish peroxidase (HRP, <0.4 mg/ml) did not. gels being obtained through HRP/H2O2...
Abstract The BET family member BRD4 is a bromodomain-containing protein that plays vital role in driving oncogene expression. Given their pivotal regulating oncogenic networks various cancer types, inhibitors (BETi) have been developed, but the clinical application has impeded by dose-limiting toxicity and resistance. Understanding mechanisms of activity identifying predictive biomarkers could facilitate successful use BETis. Herein, we show KDM5C cooperate to sustain tumor cell growth....
<div>Abstract<p>The BET family member BRD4 is a bromodomain-containing protein that plays vital role in driving oncogene expression. Given their pivotal regulating oncogenic networks various cancer types, inhibitors (BETi) have been developed, but the clinical application has impeded by dose-limiting toxicity and resistance. Understanding mechanisms of activity identifying predictive biomarkers could facilitate successful use BETis. Herein, we show KDM5C cooperate to sustain...
<p>Loss of KDM5C sensitize tumor cells to BETi treatment.</p>
<p>Compound 3b treatment enhance BETi efficacy and exhibits negligible tissue toxicity.</p>
<p>KDM5C help to maintain active state of enhancer by establishing dBiH regions.</p>
<p>KDM5C influence H3K4me3 peaks width via its histone demethylase activity.</p>
<p>KDM5C depletion significantly enhance anti-tumor activity of BETi.</p>
<p>BRD4 is a vulnerability of KDM5C deficient tumor cells.</p>
<p>BRD4 is a vulnerability of KDM5C deficient tumor cells.</p>
<p>RACK7 forms a complex with KDM5C and BRD4 contributes to chromatin recruitment.</p>
<p>KDM5C influence H3K4me3 peaks width via its histone demethylase activity.</p>
<p>PROTAC drugs compound 3b degrades KDM5C in multiples cell lines and promotes BRD4 chromatin dissociation.</p>
<div>Abstract<p>The BET family member BRD4 is a bromodomain-containing protein that plays vital role in driving oncogene expression. Given their pivotal regulating oncogenic networks various cancer types, inhibitors (BETi) have been developed, but the clinical application has impeded by dose-limiting toxicity and resistance. Understanding mechanisms of activity identifying predictive biomarkers could facilitate successful use BETis. Herein, we show KDM5C cooperate to sustain...
<p>KDM5C depletion significantly enhance anti-tumor activity of BETi.</p>
<p>Delineating KDM5C and BRD4 localization illustrating the definitions of transcriptional elements.</p>
<p>Compound 3b treatment enhance BETi efficacy and exhibits negligible tissue toxicity.</p>
<p>KDM5C help to maintain active state of enhancer by establishing dBiH regions.</p>
<p>Delineating KDM5C and BRD4 localization illustrating the definitions of transcriptional elements.</p>
<p>Loss of KDM5C sensitize tumor cells to BETi treatment.</p>
<p>Tumor cells defective in KDM5C exhibits lower BRD4 chromatin enrichment.</p>
<p>KDM5C influence H3K4me3 peaks width via its histone demethylase activity.</p>