Karen E. Beenken
Associate Professor
University of Arkansas for Medical Sciences
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Biography and Research Information
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Karen E. Beenken investigates the pathogenesis of *Staphylococcus aureus* osteomyelitis, with a particular focus on the role of extracellular proteases and the regulatory mechanisms that control their production. Her research examines how bacterial virulence factors contribute to bone infection and loss. This work includes evaluating the efficacy of bone filler scaffolds designed for local antibiotic delivery to prevent infection in contaminated bone defects.
Beenken's laboratory has explored the genetic underpinnings of *Staphylococcus aureus* virulence, specifically the function of the *sarA* gene in limiting extracellular protease production. Her publications demonstrate that the ability of *sarA* to limit protease production is critical for virulence in osteomyelitis, irrespective of the functional status of the *agr* system. She also studies how mutations in specific genes, such as *purR*, can lead to increased accumulation of virulence factors and altered protease production.
Her scholarship includes 66 publications with over 4,100 citations and an h-index of 31. Beenken has received federal funding, including a $451,739 grant from the NIH/National Institute of Allergy and Infectious Diseases, to define the role of post-translational regulation by extracellular proteases in the pathogenesis of *Staphylococcus aureus* osteomyelitis. She actively collaborates with researchers at the University of Arkansas for Medical Sciences, including Mark S. Smeltzer, Mara J. Campbell, Horace J. Spencer, and Samuel G. Mackintosh.
Metrics
- h-index: 31
- Publications: 66
- Citations: 4,142
Selected Publications
- Lipolysis of host triacylglyceride-rich lipoproteins creates a toxic microenvironment for <i>Staphylococcus aureus</i> (2026) DOI
- Staphylococcus aureus Biofilm-Associated Infections: Have We Found a Clinically Relevant Target? (2025) DOI
- Staphylococcus aureus Proteins Implicated in the Reduced Virulence of sarA and sarA/agr Mutants in Osteomyelitis (2025) DOI
- The ability of <i>sarA</i> to limit protease production plays a key role in the pathogenesis of <i>Staphylococcus aureus</i> osteomyelitis irrespective of the functional status of <i>agr</i> (2024) DOI
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis (2024) DOI
- Increased production of aureolysin and staphopain A is a primary determinant of the reduced virulence of <i>Staphylococcus aureus sarA</i> mutants in osteomyelitis (2024) DOI
- Comparative evaluation of small molecules reported to be inhibitors of <i>Staphylococcus aureus</i> biofilm formation (2023) DOI
- The major role of <i>sarA</i> in limiting <i>Staphylococcus aureus</i> extracellular protease production <i>in vitro</i> is correlated with decreased virulence in diverse clinical isolates in osteomyelitis (2023) DOI
- The major role of <i>sarA</i> in limiting <i>Staphylococcus aureus</i> extracellular protease production is correlated with decreased virulence in diverse clinical isolates in osteomyelitis (2022) DOI
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect (2021) DOI
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1 (2021) DOI
- The Increased Accumulation of Staphylococcus aureus Virulence Factors Is Maximized in a <i>purR</i> Mutant by the Increased Production of SarA and Decreased Production of Extracellular Proteases (2021) DOI
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis (2021) DOI
Federal Grants 1 $451,739 total
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