Karen E. Beenken
Associate Professor
faculty
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Biography and Research Information
OverviewAI-generated summary
Karen E. Beenken's research focuses on the pathogenesis of *Staphylococcus aureus* infections, particularly osteomyelitis. Her work investigates the role of bacterial virulence factors and host responses in disease progression. She has explored the mechanisms by which *Staphylococcus aureus* regulates protease production, including the significant role of the *sarA* gene in limiting extracellular protease activity. This regulation is linked to reduced virulence in clinical isolates relevant to osteomyelitis. Beenken also examines how mutations, such as in the *purR* gene, can lead to increased accumulation of virulence factors and altered protease production, impacting disease outcomes.
Her laboratory studies the host's contribution to bone loss during *Staphylococcus aureus* osteomyelitis, specifically investigating the requirement of RANKL-mediated osteoclast formation. Furthermore, Beenken evaluates potential therapeutic strategies, such as the use of bone filler scaffolds for local antibiotic delivery to prevent or treat *Staphylococcus aureus* infections in contaminated bone defects. Her scholarship metrics include an h-index of 31 and over 4,000 citations, reflecting a significant body of work in her field. She has received federal funding from the NIH/National Institute of Allergy and Infectious Diseases for her research on post-translational regulation by extracellular proteases in osteomyelitis pathogenesis.
Metrics
- h-index: 31
- Publications: 70
- Citations: 4,235
Selected Publications
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Lipolysis of host triacylglyceride-rich lipoproteins creates a toxic microenvironment for <i>Staphylococcus aureus</i> (2026)
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Staphylococcus aureus Biofilm-Associated Infections: Have We Found a Clinically Relevant Target? (2025)
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Staphylococcus aureus Proteins Implicated in the Reduced Virulence of sarA and sarA/agr Mutants in Osteomyelitis (2025)
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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)
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RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis (2024)
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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)
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Comparative evaluation of small molecules reported to be inhibitors of <i>Staphylococcus aureus</i> biofilm formation (2023)
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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)
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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)
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Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect (2021)
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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)
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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)
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Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis (2021)
Federal Grants 1 $451,739 total
Grants & Funding
Collaboration Network
Top Collaborators
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- 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
- 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
Showing 5 of 14 shared publications
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- 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
- Increased production of aureolysin and staphopain A is a primary determinant of the reduced virulence of <i>Staphylococcus aureus sarA</i> mutants in osteomyelitis
- 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>
Showing 5 of 9 shared publications
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1
- 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
- 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
- Increased production of aureolysin and staphopain A is a primary determinant of the reduced virulence of <i>Staphylococcus aureus sarA</i> mutants in osteomyelitis
Showing 5 of 7 shared publications
- 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
- Comparative evaluation of small molecules reported to be inhibitors of <i>Staphylococcus aureus</i> biofilm formation
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- 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
- 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
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1
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