Clara M. Stiefel
Researcher
Also affiliated: University of Kaiserslautern (2021); The University of Texas at San Antonio Health Science Center (2023)
Unknown Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Clara M. Stiefel's research focuses on the molecular mechanisms underlying genetic disorders and DNA damage repair. Her work investigates how constitutive trisomies, such as Down Syndrome, trigger cellular responses including autophagy and innate immune activation through the cGAS-STING pathway. She has also explored the role of specific nucleases, like APE2, in essential DNA double-strand break repair processes, specifically microhomology-mediated end joining. Further investigations have examined genetic variations, such as a rare SNP in the HELB gene, and their impact on protein interactions and cellular function. 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, with whom she has co-authored publications. Her scholarship metrics include an h-index of 4, with 5 total publications and 144 total citations.
Metrics
- h-index: 4
- Publications: 5
- Citations: 145
Selected Publications
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Rare SNP in the <i>HELB</i> 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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