Kristen M. Sterba
Sourced from institutional research profiles (UAMS TRI or ARA).
Associate Provost for Students and Admin
Academic Affairs, College of Medicine
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Kristen M. Sterba's research has focused on the molecular mechanisms of bacterial gene regulation, particularly within *Staphylococcus aureus*. Her work has investigated the binding sites and regulatory functions of the SarA protein, exploring its responsiveness to environmental factors such as redox potential and pH. Sterba has also examined the role of SarA in bacteriophage integration and excision processes. Additionally, her research has touched upon cellular responses to chemotherapy, specifically studying the impact of c-Jun overexpression on vinblastine resistance in MCF7 cells by influencing apoptosis and senescence pathways. More recently, Sterba's scholarship has extended to evaluating the outcomes of Ph.D. students from underrepresented racial groups in biomedical sciences, analyzing performance measures within programs like the UAMS IMSD Program.
Metrics
- h-index: 4
- Publications: 4
- Citations: 150
Selected Publications
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Performance measures of racially underrepresented Ph.D. students in biomedical sciences: The UAMS IMSD Program Outcomes (2021)
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Staphylococcus aureus SarA is a regulatory protein responsive to redox and pH that can support bacteriophage lambda integrase‐mediated excision/recombination (2009)
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Inducible overexpression of c-Jun in MCF7 cells causes resistance to vinblastine via inhibition of drug-induced apoptosis and senescence at a step subsequent to mitotic arrest (2006)
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Characterization of Staphylococcus aureus SarA Binding Sites (2003)
Grants & Funding
As listed on this researcher's institutional profile.
- The University of Arkansas for Medical Sciences Initiative for Maximizing Student Development Program NIH Co-Investigator
- COVID-19 Higher Education Emergency Relief Fund-Institutional Portion University of Arkansas for Medical Sciences US Department of Education Principal Investigator
- UAMS Summer Undergraduate Research Program to Increase Diversity in Research NIH Co-Investigator
Collaboration Network
Top Collaborators
- Characterization of Staphylococcus aureus SarA Binding Sites
- Staphylococcus aureus SarA is a regulatory protein responsive to redox and pH that can support bacteriophage lambda integrase‐mediated excision/recombination
- Characterization of Staphylococcus aureus SarA Binding Sites
- Staphylococcus aureus SarA is a regulatory protein responsive to redox and pH that can support bacteriophage lambda integrase‐mediated excision/recombination
- Staphylococcus aureus SarA is a regulatory protein responsive to redox and pH that can support bacteriophage lambda integrase‐mediated excision/recombination
- Staphylococcus aureus SarA is a regulatory protein responsive to redox and pH that can support bacteriophage lambda integrase‐mediated excision/recombination
- Staphylococcus aureus SarA is a regulatory protein responsive to redox and pH that can support bacteriophage lambda integrase‐mediated excision/recombination
- Staphylococcus aureus SarA is a regulatory protein responsive to redox and pH that can support bacteriophage lambda integrase‐mediated excision/recombination
- Inducible overexpression of c-Jun in MCF7 cells causes resistance to vinblastine via inhibition of drug-induced apoptosis and senescence at a step subsequent to mitotic arrest
- Inducible overexpression of c-Jun in MCF7 cells causes resistance to vinblastine via inhibition of drug-induced apoptosis and senescence at a step subsequent to mitotic arrest
- Inducible overexpression of c-Jun in MCF7 cells causes resistance to vinblastine via inhibition of drug-induced apoptosis and senescence at a step subsequent to mitotic arrest
- Inducible overexpression of c-Jun in MCF7 cells causes resistance to vinblastine via inhibition of drug-induced apoptosis and senescence at a step subsequent to mitotic arrest
- Inducible overexpression of c-Jun in MCF7 cells causes resistance to vinblastine via inhibition of drug-induced apoptosis and senescence at a step subsequent to mitotic arrest
- Characterization of Staphylococcus aureus SarA Binding Sites
- Characterization of Staphylococcus aureus SarA Binding Sites
- Performance measures of racially underrepresented Ph.D. students in biomedical sciences: The UAMS IMSD Program Outcomes
- Performance measures of racially underrepresented Ph.D. students in biomedical sciences: The UAMS IMSD Program Outcomes
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