Biography and Research Information
OverviewAI-generated summary
L. Rodgers' research focuses on understanding biological responses and developing novel biomaterials. Recent publications include work on modifying naturally occurring biopolymers for biomedical applications and a proteomic analysis of the DNA damage response in exhausted T cells. Rodgers has published 16 papers with 12 citations and an h-index of 2. Collaborations include shared publications with Brian Koss, Katherine Wallis, and Daniel Fil, all at the University of Arkansas for Medical Sciences. Rodgers' work involves investigating cellular mechanisms and exploring the potential of biomaterials in medical contexts.
Metrics
- h-index: 2
- Publications: 16
- Citations: 12
Selected Publications
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929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells (2024)
Collaboration Network
Top Collaborators
- Modifying Naturally Occurring, Nonmammalian-Sourced Biopolymers for Biomedical Applications
- Modifying Naturally Occurring, Nonmammalian-Sourced Biopolymers for Biomedical Applications
- Modifying Naturally Occurring, Nonmammalian-Sourced Biopolymers for Biomedical Applications
- Modifying Naturally Occurring, Nonmammalian-Sourced Biopolymers for Biomedical Applications
- Modifying Naturally Occurring, Nonmammalian-Sourced Biopolymers for Biomedical Applications
- Modifying Naturally Occurring, Nonmammalian-Sourced Biopolymers for Biomedical Applications
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
- 929 Proteomic analysis reveals differential modulation of the DNA damage response in exhausted T cells
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