Clara M. Stiefel
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Also affiliated: University of Kaiserslautern (2021); The University of Texas at San Antonio Health Science Center (2023)
Formerly Arkansas Affiliated with UAMS through 2024; recent publications list The University of Texas at San Antonio Health Science Center.
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Clara M. Stiefel's research investigates DNA damage and repair mechanisms, particularly in the context of chromosomal abnormalities. Her work examines how constitutive trisomies, such as Down syndrome, influence cellular responses to genotoxic stress, including the activation of autophagy and the innate immune system via the cGAS-STING pathway. Stiefel also studies the role of specific nucleases, like APE2, in DNA double-strand break repair pathways, including microhomology-mediated end joining. Additionally, her research explores the regulation of proteins like 53BP1 at damaged chromatin and how histone modifications impact DNA repair processes. She has published findings on the consequences of chromosome gain in trisomy syndromes and the mechanisms by which complexes like HELZ-BRCA2 resolve R-loops to facilitate homologous recombination. Stiefel collaborates with researchers at the University of Arkansas for Medical Sciences, including Maroof K. Zafar, Eric J. Enemark, Alicia K. Byrd, and Matthew D. Thompson.
Metrics
- h-index: 4
- Publications: 5
- Citations: 146
Selected Publications
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Rare SNP in the HELB gene interferes with RPA interaction and cellular function of HELB (2024)
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Consequences of chromosome gain: A new view on trisomy syndromes (2022)
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The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining (2022)
Collaboration Network
Top Collaborators
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- The APE2 nuclease is essential for DNA double strand break repair by microhomology-mediated end-joining
- Consequences of chromosome gain: A new view on trisomy syndromes
- Consequences of chromosome gain: A new view on trisomy syndromes
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
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