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- Bioorganic Chemistry and the Origins of Chemical Biology
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1. Biomimetic catalysis
- Prof. Ronald Breslow
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2. Bioorganic studies of vision
- Prof. Koji Nakanishi
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3. Perspectives on biological catalysis
- Prof. Stephen Benkovic
- Nucleic Acids and Drug/Nucleic Acid Interactions
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5. Site-specifically modified ribosomal RNAs
- Prof. Christine Chow
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7. Drug-DNA interactions of the mitomycins
- Prof. Maria Tomasz
- Protein Function and Cellular Signaling
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8. Chemical synthesis of proteins
- Prof. Lei Liu
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9. Visualizing and manipulating phosphoinositide and phospholipid signaling
- Prof. Glenn Prestwich
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11. Polydactyl zinc finger proteins: software and hardware for genomes
- Prof. Carlos Barbas
- Peptides, Small-Molecules and Chemical Diversity
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12. Chemical synthesis of peptides and peptide libraries
- Prof. Victor Hruby
- Proteomics: The Study of Biomolecules and Interactions
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13. Quantitative proteomics
- Prof. Ruedi Aebersold
- Archived Lectures *These may not cover the latest advances in the field
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15. Solid phase peptide synthesis
- Prof. Stephen Kent
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17. Tagged library for chemical genetics
- Dr. Young-Tae Chang
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18. Covalently constrained alpha-helices
- Dr. Paramjit Arora
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19. SICLOPPS: genetic system for production of backbone cyclized peptides
- Dr. Sergey Savinov
Printable Handouts
Navigable Slide Index
- Introduction
- Overview
- Oxidative stress
- Antioxidants
- Oxidative damage
- Oxidative damage to nucleic acids
- Approach to study oxidative damage
- Radical precursor synthesis
- Selective radical generation
- Photochemical radical generation
- Method overview
- Novel method for reverse automated RNA synthesis using H-phosphonate chemistry
- H-phosphonates
- Nucleic acid synthesis
- Commercially available monomers
- Automated synthesis
- Post synthetic manipulations (1)
- 5' H-phosphonate monomers
- Synthesis of 5' H-phosphonate
- Proposed automated synthesis
- Post synthetic manipulations (2)
- Reverse automated RNA method
- Conclusions
- Acknowledgement
Topics Covered
- An introduction to oxidative stress
- Sources of oxidative damage
- Removal of radicals with antioxidants
- Oxidative damage to nucleic acids
- Methodology to investigate oxidative damage
- Radicals generation
- H-phosphonates
- Reverse automated RNA methodology
Talk Citation
Bedi, M. (2021, July 28). Creation of tools for the investigation of oxidative damage to nucleic acids [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 2, 2025, from https://doi.org/10.69645/NMBL9685.Export Citation (RIS)
Publication History
- Published on July 28, 2021
Financial Disclosures
- The work presented in the talk was supported by funding from the national science foundation: Award #1904754: Creation of tools to determine the impact of natural modifications on RNA damage Award #0848303: Creation of Tools for the Study of Reactive Intermediates in DNA and RNA.
A selection of talks on Biochemistry
Transcript
Please wait while the transcript is being prepared...
0:00
Hello, my name is Mel Bedi,
and today I'll be speaking to you on the subject of the creation of
tools for the investigation of oxidative damage to nucleic acids.
0:12
We'll begin this talk by providing
a brief introductory background on oxidative stress, and its implications.
We will then take a look at the approach that the Bryant-Friedrich group takes
in the creation of tools to study oxidative damage involving nucleic acids.
Finally, we'll discuss a novel method for reverse
automated RNA synthesis, employing H-phosphonate chemistry.
Let's begin with our introduction on oxidative stress.
0:41
Oxidative stress is one of the major contributors to the endogenous exposome.
It is a condition that arises when the proliferation of
reactive oxygen species (ROS) overwhelms the cell's ability to detoxify them.
This leads to damage to cellular components.
Sources of reactive oxygen species are both endogenous and exogenous.
Endogenously, reactive oxygen species can be
produced and released by the endoplasmic reticulum,
the mitochondria, the peroxisome, and the macrophages.
Some of the exogenous sources of reactive oxygen species include UV light from the sun,
ionizing radiation, and environmental pollutants.
At the cellular level, the proliferation of reactive oxygen species during
oxidative stress can cause damage to all the macromolecules,
including lipids, proteins, DNA, and RNA.
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