Sang Eun Lee
University of Texas Health Science Center at San Antonio, TX·Genetics
Some cancer drugs and environmental pollutants cause proteins to become stuck to DNA. These DNA–protein crosslinks (DPCs) block nearly every process that reads or copies DNA.
- Fields
Genetics
Biochemistry
Biology
- Topics
DNA repair
DNA-protein crosslinks
Apn2
- Grants
- 1 known grant, through Feb 2027
What they work on
- Determine how the conserved DNA-repair enzyme Apn2 recognizes and removes many different chemical blocks at DNA 3' ends, including cyclic phosphates and tyrosine–DNA links, using genetic and biochemical assays in yeast.
- Define how Apn2's 3' end-cleaning activity is regulated in different cellular and functional contexts.
- Test the importance of Apn2 and human APE2 in removing trapped topoisomerase I from DNA in cells exposed to chemotherapy drugs.
- Identify the proteases that work with Apn2 to remove DNA–protein crosslinks formed by environmental pollutants and chemicals.
More about the research
If cells do not remove them quickly, they cause mutations, genome instability and cell death. Cells have several ways to clear these blockages, but one route, in which a protease cuts up the stuck protein and a nuclease cuts the remaining peptide–DNA bond, is poorly understood. Accumulated DPCs have been linked to aging, neurodegeneration and liver cancer.
Why it matters
Human APE2 is essential for the survival of BRCA-deficient breast and ovarian cancer cells. Understanding how it clears trapped proteins could therefore help explain or overcome therapy resistance in these cancers. The work may also clarify how failed repair of protein–DNA crosslinks contributes to motor neuron diseases, aging-related neurodegeneration and liver cancer.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jaime Lopez-Mosqueda
University of Texas at Austin, TX·Biochemistry·Early-career
Test for a unifying molecular mark that flags DNA-protein crosslinks for destruction, regardless of the size or chemical nature of the trapped protein, using biochemical and molecular biology approaches.
Dale A Ramsden
University of North Carolina at Chapel Hill, NC·Biochemistry
Determine how Pol θ's interactions with the DNA-copying machinery, including the polymerase Pol δ and the DNA clamp PCNA, affect cells' need for Pol θ-mediated end joining.
Juan Lucas Argueso
Colorado State University-Fort Collins, CO·Genetics
Measure rates of copy number variation (CNV), loss of heterozygosity (LOH), and whole-chromosome gain or loss in dividing and meiotic budding yeast cells, using custom, highly sensitive cell-based assays.
The school
University of Texas Health Science Center at San Antonio: 15 labs on PI Pages, $313M a year on research, 149 research doctorates a year.
More about University of Texas Health Science Center at San Antonio
Reach out
A start for your email. Fill in the brackets.