Presentation Title

Modified PNA Oligomers as a Method for Recognition of Mutant Non-Coding RNA

Location

Atrium

Session Format

Poster Presentation

Research Area Topic:

Natural & Physical Sciences - Chemistry

Co-Presenters, Co- Authors, Co-Researchers, Mentors, or Faculty Advisors

Dr. Arambula

faculty advisor

Abstract

Trinucleotide Repeat Expansion Disorders (TREDS) are ascribed to generational expansion of genomic repeats. In many cases, these genomic repeats are transcribed to non-coding regions at the RNA level resulting in novel loss of function mechanisms. In this presentation, we propose and present preliminary work on the ability of modified PNA oligomers as a means of RNA and DNA repeat recognition using CUG/CTG repeats (Myotonic Dystrophy type 1) as a model. We propose that by binding to the mutant RNA, the PNA would inhibit non-natural RNA-protein binding events at specific trinucleotide repeats which is considered to be the direct cause of myotonic dystrophy type 1. If efficient, the findings of this research may lead to a new class of compounds that will provide treatment for genetic diseases that are caused by mutant RNA.

Keywords

Myotonic dystrophy, Acridine, Peptide nucleic acid, Trinucleotide repeat expansion disorders

Presentation Type and Release Option

Presentation (Open Access)

Start Date

4-24-2015 2:45 PM

End Date

4-24-2015 4:00 PM

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Apr 24th, 2:45 PM Apr 24th, 4:00 PM

Modified PNA Oligomers as a Method for Recognition of Mutant Non-Coding RNA

Atrium

Trinucleotide Repeat Expansion Disorders (TREDS) are ascribed to generational expansion of genomic repeats. In many cases, these genomic repeats are transcribed to non-coding regions at the RNA level resulting in novel loss of function mechanisms. In this presentation, we propose and present preliminary work on the ability of modified PNA oligomers as a means of RNA and DNA repeat recognition using CUG/CTG repeats (Myotonic Dystrophy type 1) as a model. We propose that by binding to the mutant RNA, the PNA would inhibit non-natural RNA-protein binding events at specific trinucleotide repeats which is considered to be the direct cause of myotonic dystrophy type 1. If efficient, the findings of this research may lead to a new class of compounds that will provide treatment for genetic diseases that are caused by mutant RNA.