A5102924878- Computational Drug Discovery Methods
- Hematopoietic Stem Cell Transplantation
- Genetics, Bioinformatics, and Biomedical Research
- Extracellular vesicles in disease
- DNA Repair Mechanisms
- Synthesis and biological activity
- Mesenchymal stem cell research
- Cancer Genomics and Diagnostics
Palo Alto University
2025
Stanford University
2024-2025
Army Medical University
2023
Chongqing Medical University
2023
Second Affiliated Hospital of Chongqing Medical University
2023
Dalian Medical University
2023
Rationale:In the bone marrow microenvironment (BMME), mesenchymal stem/stromal cells (MSCs) control self-renewal of both healthy and cancerous hematopoietic stem/progenitor (HSPCs).We previously showed that in vivo leukemia-derived MSCs change neighbor into leukemia-permissive states boost leukemia cell proliferation, survival, chemotherapy resistance.But mechanisms behind how state changes are still not fully understood.Methods: Here, we took a reverse engineering approach to determine...
Abstract The amplification of oncogenes on extrachromosomal DNA (ecDNA) is common in cancer and associated with poor outcomes. Uneven inheritance ecDNA during cell division leads to intratumoral copy number heterogeneity. However, the relationship between shifts rapid environmental adaptation cells remains unclear. In this study, we utilized imaging single-cell multi-omics analyses demonstrate that transcript protein expression oncogenes, along functional heterogeneity, correlate Using...
Abstract Extrachromosomal DNA (ecDNA) presents a major challenge for precision medicine, contributing to poor survival patients with oncogene-amplified tumours. EcDNA renders tumours resistant targeted treatments by facilitating massive transcription of oncogenes and rapid genome evolution. At present, there are no ecDNA- specific treatments. Here we show that enhancing replication conflict enables elimination ecDNA-containing cancers, exposing an actionable vulnerability. Stepwise analyses...
In animals, heterotrimeric guanine nucleotide-binding protein (G protein) signaling is initiated by G protein-coupled receptors (GPCRs), which activate subunits.By contrast, the plant Arabidopsis thaliana lacks canonical GPCRs.Its subunit (AtGPA1) self-activating in absence of any receptor or nucleotide exchange factor and features both faster binding GTP slower hydrolysis when compared to mammalian G{alpha} proteins.Receptor-independent proteins must have a fundamentally different mechanism...