A5042302391- Epigenetics and DNA Methylation
- Pluripotent Stem Cells Research
- Mitochondrial Function and Pathology
- Chromatin Remodeling and Cancer
- Cancer Genomics and Diagnostics
- Protein Degradation and Inhibitors
- Histone Deacetylase Inhibitors Research
- Autophagy in Disease and Therapy
- Viral Infections and Immunology Research
- Cardiac electrophysiology and arrhythmias
- Molecular Biology Techniques and Applications
- Brain Tumor Detection and Classification
- Glioma Diagnosis and Treatment
- Macrophage Migration Inhibitory Factor
- Protein Kinase Regulation and GTPase Signaling
- Ion channel regulation and function
- interferon and immune responses
- Inflammasome and immune disorders
- RNA modifications and cancer
- Immune Response and Inflammation
- Health Sciences Research and Education
- Neuroscience and Neuropharmacology Research
- Advanced Power Amplifier Design
- Atherosclerosis and Cardiovascular Diseases
- Signaling Pathways in Disease
Southern Medical University
2025
Harbin Medical University
2022-2024
Beijing Fengtai Hospital
2024
Weatherford College
2023
<p>Supplementary Figures S1 shows that GSCs produce high levels of phosphocreatine through upregulating CKB. Supplementary S2 ZEB1 promotes CKB transcription in GSCs. S3 knockdown impedes GBM growth. S4 disruption production S5 cCr treatment no side effect on mice. S6 binds to BRD2 and inhibits its ubiquitin mediated proteasomal degradation. S7 chromosome segregation GSC proliferation transcription. S8 biosynthesis by improves JQ1 therapeutic efficacy GBM.</p>
<p>Supplementary Figures S1 shows that GSCs produce high levels of phosphocreatine through upregulating CKB. Supplementary S2 ZEB1 promotes CKB transcription in GSCs. S3 knockdown impedes GBM growth. S4 disruption production S5 cCr treatment no side effect on mice. S6 binds to BRD2 and inhibits its ubiquitin mediated proteasomal degradation. S7 chromosome segregation GSC proliferation transcription. S8 biosynthesis by improves JQ1 therapeutic efficacy GBM.</p>
Glioblastoma (GBM) exhibits profound metabolic plasticity for survival and therapeutic resistance, while the underlying mechanisms remain unclear. Here, we show that GBM stem cells reprogram epigenetic landscape by producing substantial amounts of phosphocreatine (PCr). This production is attributed to elevated transcription brain-type creatine kinase, mediated Zinc finger E-box binding homeobox 1. PCr inhibits poly-ubiquitination chromatin regulator bromodomain containing protein 2 (BRD2)...
To investigate the effect of mogroside IIIE (MGIIIE) on isoproterenol (ISO)-induced myocardial fibrosis and explore its possible mechanisms.Forty C57BL/6 male mice (6-8 weeks) were randomly divided into a control group (n=10), model low MGIIIE dose high (n=10). Myocardial was established by subcutaneous ISO injection. After 2 weeks continuous gastric administration MGIIIE, cardiac structure evaluated echocardiography. inflammation histology examination. Toll-like receptor 4 (TLR4), myeloid...
Ivabradine (IVA) reduces heart rate by inhibiting hyperpolarization-activated cyclic nucleotide-gated channels (HCNs), which play a role in the promotion of pacemaker activity cardiac sinoatrial node cells. HCNs are highly expressed neural and myocardial tissues involved modulation inflammatory neuropathic pain. However, whether IVA exerts any effect on inflammation pathogenesis failure is unclear. We employed single-cell RNA sequencing (scRNA-seq) porcine myosin-induced experimental...
Artemisinin and its derivatives, the well-known anti-malarial drugs extracted from traditional Chinese medicine, Artemisia annua, have been implicated in treating fibrotic diseases. However, whether artemisinin affects cardiac fibrosis pathogenesis of heart failure is still unknown. This study aimed to evaluate possible effects on function myocardial model explore underlying mechanisms.
The metabotropic glutamate receptor 5 (mGlu5) is a Class C G protein-coupled receptor, ubiquitously expressed throughout the CNS. With major roles in cognition, learning and memory, mGlu5 dysfunction linked with numerous neurodegenerative neuropsychiatric disorders, presenting viable therapeutic target. Allosteric modulators bind topographically distinct sites from other orthosteric agonists enhance (positive allosteric modulators, PAMs), inhibit (negative NAMs) or do not effect (neutral...