Research output per year
Research output per year
Personal profile
Research interests
Our DNA is susceptible to damage based on our lifestyle, environmental exposures, and even cancer treatments. Using a combination of structural biology, biochemical, and cell-biology techniques we explore the interplay between DNA damage, DNA repair, and the transcriptional regulation of cancer-related genes. We hope, by researching DNA repair, to pave the way for the development of therapeutics that can selectively enhance or stop DNA repair based on a patient’s need.
Our cells are continuously exposed to DNA-damaging agents, including what we eat and drink, the air we breathe, exposure to the sun, as well as DNA-damaging cancer treatments. In the case of DNA-damaging cancer treatments, the goal is for the DNA damage to selectively kill cancer cells without being inhibited by the cells DNA repair mechanisms. However, in other cases, you need to enhance DNA repair to prevent cancer-causing mutations. Thus, by researching DNA repair, we hope to develop therapeutic strategies to selectively enhance or reduce DNA repair depending on a patient’s need.
Projects in the Whitaker lab aim to elucidate the molecular mechanisms coupling two key biological responses to oxidative DNA damage within G-quadruplex forming sequences. Specifically, base excision repair (BER) and the epigenic-like transcriptional regulation of key tumor suppressors and oncogenes. The long-term goal is to identify molecular targets that can be exploited to improve cancer therapies.
The primary techniques utilized in the lab include structural biology (X-ray crystallography, Cryo-EM), nucleic acid enzymology, single-molecule fluorescence microscopy, as well as human cell-based assays.
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Collaborations and top research areas from the last five years
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Oxidative DNA damage on the VEGF G-quadruplex forming promoter is repaired via long-patch BER
Hussen, A. S., Kravitz, H. L., Freudenthal, B. D. & Whitaker, A. M., Apr 2024, In: Environmental and Molecular Mutagenesis. 65 Suppl 1, Suppl 1, p. 25-39 15 p.Research output: Contribution to journal › Article › peer-review
Open Access4 Scopus citations -
A two-residue nascent-strand steric gate controls synthesis of 2′-O-methyl- and 2′-O-(2-methoxyethyl)-RNA
Freund, N., Taylor, A. I., Arangundy-Franklin, S., Subramanian, N., Peak-Chew, S. Y., Whitaker, A. M., Freudenthal, B. D., Abramov, M., Herdewijn, P. & Holliger, P., Jan 2023, In: Nature Chemistry. 15, 1, p. 91-100 10 p.Research output: Contribution to journal › Article › peer-review
Open Access40 Scopus citations -
Processing oxidatively damaged bases at DNA strand breaks by APE1
Whitaker, A. M., Stark, W. J. & Freudenthal, B. D., Sep 9 2022, In: Nucleic Acids Research. 50, 16, p. 9521-9533 13 p.Research output: Contribution to journal › Article › peer-review
Open Access16 Scopus citations -
Construction of a three-color prism-based tirf microscope to study the interactions and dynamics of macromolecules
Fairlamb, M. S., Whitaker, A. M., Bain, F. E., Spies, M. & Freudenthal, B. D., May 23 2021, In: Biology. 10, 7, 571.Research output: Contribution to journal › Article › peer-review
Open Access9 Scopus citations -
AP-endonuclease 1 sculpts DNA through an anchoring tyrosine residue on the DNA intercalating loop
Hoitsma, N. M., Whitaker, A. M., Beckwitt, E. C., Jang, S., Agarwal, P. K., Van Houten, B. & Freudenthal, B. D., Jul 27 2020, In: Nucleic Acids Research. 48, 13, p. 7345-7355 11 p.Research output: Contribution to journal › Article › peer-review
Open Access27 Scopus citations
Press/Media
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Fox Chase Researcher Receives Grant to Explore How to Indirectly Target Signaling Protein in Pancreatic Cancer
01/23/24
1 item of Media coverage
Press/Media
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Fox Chase Study Reveals Mechanism for Repairing DNA Damage Caused by Environmental Triggers
11/17/22
1 item of Media coverage
Press/Media
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