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Articles 1 - 4 of 4
Full-Text Articles in Translational Medical Research
Epigenetic Alterations Mediate Ipsc Normalization Of Dna-Repair Expression And Tnr Stability In Huntington's Disease, Peter A. Mollica, Martina Zamponi, John Reid, Deepak Sharma, Alyson E. White, Roy C. Ogle, Robert D. Bruno, Patrick C. Sachs
Epigenetic Alterations Mediate Ipsc Normalization Of Dna-Repair Expression And Tnr Stability In Huntington's Disease, Peter A. Mollica, Martina Zamponi, John Reid, Deepak Sharma, Alyson E. White, Roy C. Ogle, Robert D. Bruno, Patrick C. Sachs
School of Medical Diagnostics & Translational Sciences Faculty Publications
Huntington's disease (HD) is a rare autosomal dominant neurodegenerative disorder caused by a cytosine-adenine-guanine (CAG) trinucleotide repeat (TNR) expansion within the HTT gene. The mechanisms underlying HD-associated cellular dysfunction in pluripotency and neurodevelopment are poorly understood. We had previously identified downregulation of selected DNA repair genes in HD fibroblasts relative to wild-type fibroblasts, as a result of promoter hypermethylation. Here, we tested the hypothesis that hypomethylation during cellular reprogramming to the induced pluripotent stem cell (iPSC) state leads to upregulation of DNA repair genes and stabilization of TNRs in HD cells. We sought to determine how the HD TNR region …
Genotype-Specific Insertion Of Cytotoxic Genetic Elements Into Cancer Cells, Ryan Englander
Genotype-Specific Insertion Of Cytotoxic Genetic Elements Into Cancer Cells, Ryan Englander
University Scholar Projects
The new gene editing system CRISPR/Cas9, composed of a complex composed of a guide RNA and the Cas9 endonuclease, promises to revolutionize biological research and potentially allow clinicians to directly modify patient DNA in vivo. While its applications in the treatment of genetic diseases and in modifying immune cells for immunotherapy are currently being explored, CRISPR/Cas9’s potential utility as a modular system for targeting tumor-specific mutated sequences has not as of yet been explored. While CRISPR/Cas9 is specific enough to target small insertions and deletions or gross chromosomal rearrangements, it is not specific enough to reliably restrict editing to …
The Pharmacogene Variation (Pharmvar) Consortium: Incorporation Of The Human Cytochrome P450 (Cyp) Allele Nomenclature Database, Andrea Gaedigk, Magnus Ingelman-Sundberg, Neil A. Miller, J Steven Leeder, Michelle Whirl-Carrillo, Teri E. Klein
The Pharmacogene Variation (Pharmvar) Consortium: Incorporation Of The Human Cytochrome P450 (Cyp) Allele Nomenclature Database, Andrea Gaedigk, Magnus Ingelman-Sundberg, Neil A. Miller, J Steven Leeder, Michelle Whirl-Carrillo, Teri E. Klein
Manuscripts, Articles, Book Chapters and Other Papers
The Human Cytochrome P450 (CYP) Allele Nomenclature Database, a critical resource to the pharmacogenetics and genomics communities, will be transitioning to the Pharmacogene Variation (PharmVar) Consortium. In this report we provide a summary of the current database, provide an overview of the PharmVar consortium and highlight the PharmVar database which will serve as the new home for pharmacogene nomenclature.
Electrotransfer Of Different Control Plasmids Elicits Different Antitumor Effectiveness In B16.F10 Melanoma, Masa Bosnjak, Tanjo Jesenko, Urska Kamensek, Gregor Sersa, Jaka Lavrencak, Loree Heller, Maja Cemazar
Electrotransfer Of Different Control Plasmids Elicits Different Antitumor Effectiveness In B16.F10 Melanoma, Masa Bosnjak, Tanjo Jesenko, Urska Kamensek, Gregor Sersa, Jaka Lavrencak, Loree Heller, Maja Cemazar
Bioelectrics Publications
Several studies have shown that different control plasmids may cause antitumor action in different murine tumor models after gene electrotransfer (GET). Due to the differences in GET protocols, plasmid vectors, and experimental models, the observed antitumor effects were incomparable. Therefore, the current study was conducted comparing antitumor effectiveness of three different control plasmids using the same GET parameters. We followed cytotoxicity in vitro and the antitumor effect in vivo after GET of control plasmids pControl, pENTR/U6 scr and pVAX1 in B16.F10 murine melanoma cells and tumors. Types of cell death and upregulation of selected cytosolic DNA sensors and cytokines were …