Publications by authors named "Michael Skogen"
Article Synopsis
- Huntington's Disease (HD) is a genetic disorder caused by misfolded mutant huntingtin protein that disrupts normal cellular functions and leads to neuronal degeneration.
- Recent research has identified short guanosine monotonic oligonucleotides, specifically a 20-mer all G-oligonucleotide (HDG), which can inhibit the aggregation of the mutant protein and promote cell survival in test conditions.
- The findings suggest that these G-quartet oligonucleotides could represent a novel therapeutic strategy to combat Huntington's Disease by targeting the protein aggregation that contributes to the disease's progression.
A tolerance of DNA heterology in the mammalian targeted gene repair reaction.
Oligonucleotides
November 2005
Targeted gene repair consists of at least two major steps, the pairing of an oligonucleotide to a site bearing DNA sequence complementarity followed by a nucleotide exchange reaction directed by the oligonucleotide. In this study, oligonucleotides with different structures were designed to target a stably integrated (mutant) enhanced green fluorescent protein (EGFP) gene and used to direct the repair of a single base mutation. We show that the efficiency of correction is influenced by the degree of DNA sequence homology existing between the oligonucleotide and target gene.
View Article and Find Full Text PDFTargeted gene repair uses short DNA oligonucleotides to direct a nucleotide exchange reaction at a designated site in a mammalian chromosome. The widespread use of this technique has been hampered by the inability of workers to achieve robust levels of correction. Here, we present a mammalian cell system in which DLD-1 cells bearing integrated copies of a mutant eGFP gene are repaired by modified single-stranded DNA oligonucleotides.
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