A5082840733- Pluripotent Stem Cells Research
- Extracellular vesicles in disease
- MicroRNA in disease regulation
- RNA regulation and disease
- RNA Interference and Gene Delivery
- RNA Research and Splicing
- Neurological disorders and treatments
- Hedgehog Signaling Pathway Studies
- Histone Deacetylase Inhibitors Research
- Ubiquitin and proteasome pathways
- Parkinson's Disease Mechanisms and Treatments
- Protein Degradation and Inhibitors
- CRISPR and Genetic Engineering
- 3D Printing in Biomedical Research
- Neurogenesis and neuroplasticity mechanisms
University of California, Berkeley
2021-2024
Research Network (United States)
2024
University of Connecticut
2017-2019
Parkinson's disease (PD) is a neurodegenerative disorder caused by complex genetic and environmental factors. Genome-edited human pluripotent stem cells (hPSCs) offer the uniique potential to advance our understanding of PD etiology providing disease-relevant cell-types carrying patient mutations along with isogenic control cells. To facilitate this experimental approach, we generated collection 55 cell lines genetically engineered harbor in genes associated monogenic (SNCA A53T, SNCA A30P,...
Summary Parkinson’s disease (PD) is a devastating neurodegenerative disorder, with both genetic and environmental causes. Human studies have identified ∼20 inherited familial genes that cause monogenic forms of PD. We investigated the effects individual PD mutations by developing medium-throughput platform using genome-editing to install in human pluripotent stem cells (hPSCs) we subsequently differentiated into midbrain lineage including dopaminergic (DA) neurons cell culture. Both global...
Abstract We used a new mouse model to better understand the cellular and molecular determinants of tumors driven by C11orf95-RELA fusion. Our approach makes use in utero electroporation binary transposase system introduce human sequence, wild type mutant, into neural progenitors, drive expression fusion different glial neuronal progenitor cell types. results indicate that truncations or point mutations C11orf95 sequence which interfere with nuclear localization result complete loss...
Abstract We used a recently developed mouse model to better understand the cellular and molecular determinants of tumors driven by oncogenic fusion protein C11orf95-RELA. Our approach makes use in utero electroporation binary transposase system introduce human C11orf95-RELA sequence, wild type mutant forms, into neural progenitors. single cell RNA-seq profile constituents within resulting mice. find that approximately 70% cells do not express oncogene these non-oncogene expressing are...
Abstract We used a recently developed mouse model to better understand the cellular and molecular determinants of tumors driven by oncogenic fusion protein C11orf95-RELA. Our approach makes use in utero electroporation binary transposase system introduce human C11orf95-RELA sequence, wild type mutant forms, into neural progenitors. single cell RNA-seq profile constituents within resulting mice. find that approximately 70% cells do not express oncogene these non-oncogene expressing are...