Karen E. Beenken
Associate Professor
Also affiliated: Southern Illinois University Carbondale (2001); Rhodes College (2017); United States Department of Health and Human Services (2005); Zimmer Biomet (United States) (2016); Bipar (2001); Creative Research Enterprises (United States) (2016); University of Memphis (2016–2017)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
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. Beenken has published research on the impact of bacterial gene regulation, such as the *sarA* locus, on the production of extracellular proteases and their subsequent effect on virulence in various clinical isolates of *Staphylococcus aureus*.
Her laboratory also examines the host's role in osteomyelitis, including the mechanisms of bone loss mediated by osteoclast formation. Beenken has received funding from the National Institute of Allergy and Infectious Diseases (NIAID) for research defining the role of post-translational regulation by extracellular proteases in the pathogenesis of *Staphylococcus aureus* osteomyelitis. Collaborations with researchers at the University of Arkansas for Medical Sciences, including Mark S. Smeltzer and Mara J. Campbell, have contributed to her publication record.
With an h-index of 31 and over 4,000 citations, Beenken is recognized as a highly cited researcher. Her work has implications for understanding and potentially targeting *Staphylococcus aureus* biofilm-associated infections and developing strategies for preventing and treating bone infections.
Metrics
- h-index: 32
- Publications: 72
- Citations: 4,290
Selected Publications
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Scaling of Neuronal Growth and Excitability Through Separable mTORC1 and mTORC2 Pathways (2026)
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A transcriptomic-driven segmentation and cell simulation framework for high-resolution spatial transcriptomics and cell-cell communication (2026)
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Mechanistic insights into the pathogenesis and therapeutic recalcitrance of <i>Staphylococcus aureus</i> osteomyelitis (2026)
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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)
Federal Grants 1 $451,739 total
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Regulation of biofilm formation in clinical isolates of Staphylococcus aureus NIH
- Detection, diagnosis and treatment of musculoskeletal infection NIH
- A nanotherapeutic approach to combat staphylococcal biofilm-associated infection NIH
- Advanced Development and Testing of a Nanomaterial-Based Scaffold for Bone Regeneration and Drug Delivery U.S. Army Medical Research & Material Command via University of Arkansas at Little Rock
- Center for Microbial Pathogenesis and Host Inflammatory Responses NIH
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
- 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
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus 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 13 shared publications
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- 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
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus 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 8 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 6 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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