Mari Davidson
Sourced from institutional research profiles (UAMS TRI or ARA).
Associate Professor
Faculty Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Mari Davidson's research focuses on understanding the molecular mechanisms underlying microbial infections and diseases. Her work investigates how pathogens interact with host cells and the host's immune response. This research contributes to the development of new diagnostic tools and therapeutic strategies for infectious diseases, with potential applications in public health and clinical medicine.
Metrics
- h-index: 23
- Publications: 51
- Citations: 1,722
Selected Publications
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Agar lot-specific inhibition in the plating efficiency of yeast spores and cells (2024)
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Creating Meiotic Recombination-Regulating DNA Sites by SpEDIT in Fission Yeast Reveals Inefficiencies, Target-Site Duplications, and Ectopic Insertions (2024)
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Laboratory horror stories: Poison in the agars (2024)
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Adaptive Control of the Meiotic Recombination Landscape by DNA Site-dependent Hotspots With Implications for Evolution (2022)
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Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways (2022)
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Molecular mechanisms for environmentally induced and evolutionarily rapid redistribution (plasticity) of meiotic recombination (2021)
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Molecular mechanisms for environmentally induced plasticity in the positioning of meiotic recombination at hotspots (2020)
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Targeted Forward Genetics: Population-Scale Analyses of Allele Replacements Spanning Thousands of Base Pairs in Fission Yeast (2019)
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Diverse DNA Sequence Motifs Activate Meiotic Recombination Hotspots Through a Common Chromatin Remodeling Pathway (2019)
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The Syphilis Testing Result Interprofessional Counseling and Education (STRICE) simulation (2019)
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Incorporating Interprofessional Education to Distance Curricula Through Online Simulation: A Pilot Project (2018)
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Chromatin-mediated regulators of meiotic recombination revealed by proteomics of a recombination hotspot (2018)
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Proteomic analysis of a meiotic recombination hotspot (2016)
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Nonsense codon suppression in fission yeast due to mutations of tRNASer.11 and translation release factor Sup35 (eRF3) (2014)
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A Stress-Activated, p38 Mitogen-Activated Protein Kinase–ATF/CREB Pathway Regulates Posttranscriptional, Sequence-Dependent Decay of Target RNAs (2013)
Grants & Funding
As listed on this researcher's institutional profile.
- Biochemistry of recombination in meiosis NIH
- Molecular mechanisms of aneuploidy NIH
- CADHERIN 5 AND ENDOTHELIAL JUNCTION NIH
Collaboration Network
Top Collaborators
- Molecular mechanisms for environmentally induced and evolutionarily rapid redistribution (plasticity) of meiotic recombination
- Adaptive Control of the Meiotic Recombination Landscape by DNA Site-dependent Hotspots With Implications for Evolution
- Laboratory horror stories: Poison in the agars
- Agar lot-specific inhibition in the plating efficiency of yeast spores and cells
- Creating Meiotic Recombination-Regulating DNA Sites by SpEDIT in Fission Yeast Reveals Inefficiencies, Target-Site Duplications, and Ectopic Insertions
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Laboratory horror stories: Poison in the agars
- Creating Meiotic Recombination-Regulating DNA Sites by SpEDIT in Fission Yeast Reveals Inefficiencies, Target-Site Duplications, and Ectopic Insertions
- Molecular mechanisms for environmentally induced and evolutionarily rapid redistribution (plasticity) of meiotic recombination
- Adaptive Control of the Meiotic Recombination Landscape by DNA Site-dependent Hotspots With Implications for Evolution
- Laboratory horror stories: Poison in the agars
- Agar lot-specific inhibition in the plating efficiency of yeast spores and cells
- Molecular mechanisms for environmentally induced and evolutionarily rapid redistribution (plasticity) of meiotic recombination
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
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