Minkyu Kim
Assistant Professor, BIO5 Institute
Assistant Professor, Biomedical / Materials Science Engineer
Assistant Professor, Biomedical Engineering
Member of the Graduate Faculty
Primary Department
Department Affiliations
(520) 621-6070
Work Summary
Minkyu Kim's research interests are in the areas of biopolymers and biomaterials for advanced national defense and healthcare. He is currently working to develop functional biopolymer materials for the treatment of antimicrobial-resistance diseases, atherosclerosis, and cell downgrowth between the skin and osseointegrated implants.
Research Interest
Minkyu Kim, Ph.D., is an Assistant Professor in the Department of Materials Science and Engineering and the Department of Biomedical Engineering at the University of Arizona. He received a Ph.D. (2011) in Mechanical engineering and Materials Science at Duke University (advisor: Prof. Marszalek). He was a postdoc at MIT from 2012 to 2016, and worked in the Bioinspired and Biofunctional Polymers group led by Prof. Olsen. Dr. Kim’s research is focused on the design and development of biopolymer-based functional materials for targeted applications in healthcare and for national defense. Based on his diverse research experiences in the areas of biopolymer nanomechanics, polymer physics and self-assembly, biomolecular engineering and soft materials, his group is currently developing (a) mechanically responsive soft materials that mimic reversible deformability of red blood cells and that can be utilized as targeted drug delivery vehicles for the early treatment of atherosclerosis, (b) nuclear membrane inspired biopolymer materials that selectively filter and neutralize a broad range of bacteria, fungi and viruses for pharmaceutical, food safety, water decontamination and defense applications, and (c) biomimetic hypoimmunogenic coatings to improve the outcomes of osseointegrated implants. Lab Website: http://kim.lab.arizona.edu

Publications

Kim, M., Wang, C., Benedetti, F., & Marszalek, P. E. (2012). A nanoscale force probe for gauging intermolecular interactions. Angewandte Chemie (International ed. in English), 51(8), 1903-6.
Kim, M., Chen, W. G., Kang, J. W., Glassman, M. J., Ribbeck, K., & Olsen, B. D. (2015). Artificially Engineered Protein Hydrogels Adapted from the Nucleoporin Nsp1 for Selective Biomolecular Transport. Advanced materials (Deerfield Beach, Fla.), 27(28), 4207-12.
Jiang, Y., Rabbi, M., Kim, M., Ke, C., Lee, W., Clark, R. L., Mieczkowski, P. A., & Marszalek, P. E. (2009). UVA generates pyrimidine dimers in DNA directly. Biophysical journal, 96(3), 1151-8.

There is increasing evidence that UVA radiation, which makes up approximately 95% of the solar UV light reaching the Earth's surface and is also commonly used for cosmetic purposes, is genotoxic. However, in contrast to UVC and UVB, the mechanisms by which UVA produces various DNA lesions are still unclear. In addition, the relative amounts of various types of UVA lesions and their mutagenic significance are also a subject of debate. Here, we exploit atomic force microscopy (AFM) imaging of individual DNA molecules, alone and in complexes with a suite of DNA repair enzymes and antibodies, to directly quantify UVA damage and reexamine its basic mechanisms at a single-molecule level. By combining the activity of endonuclease IV and T4 endonuclease V on highly purified and UVA-irradiated pUC18 plasmids, we show by direct AFM imaging that UVA produces a significant amount of abasic sites and cyclobutane pyrimidine dimers (CPDs). However, we find that only approximately 60% of the T4 endonuclease V-sensitive sites, which are commonly counted as CPDs, are true CPDs; the other 40% are abasic sites. Most importantly, our results obtained by AFM imaging of highly purified native and synthetic DNA using T4 endonuclease V, photolyase, and anti-CPD antibodies strongly suggest that CPDs are produced by UVA directly. Thus, our observations contradict the predominant view that as-yet-unidentified photosensitizers are required to transfer the energy of UVA to DNA to produce CPDs. Our results may help to resolve the long-standing controversy about the origin of UVA-produced CPDs in DNA.

Kim, D., Novak, M. T., Wilkins, J., Kim, M., Sawyer, A., & Reichert, W. M. (2007). Response of monocytes exposed to phagocytosable particles and discs of comparable surface roughness. Biomaterials, 28(29), 4231-9.

This in vitro study characterized the temporal cytokine expression profile from human monocytes exposed to phagocytosable Ti particles (0.78+/-0.12 microm) and to Ti discs of comparable surface roughness. Human THP-1 monocytes were cultured in six well tissue culture polystyrene (TCPS) plates. Each well was either bare, contained Ti particles (the particles were clearly engulfed by the monocytes), or contained a Ti disc. Half of the wells were treated with 1 microg/mL lipopolysaccharide (LPS), while the other half were left unstimulated. Unstimulated and LPS-stimulated cells in bare wells were the negative and positive controls, respectively. Supernatant was sampled from each well at 1, 6, 24, 48, and 72 h and assayed for the expression of nine different cytokines using a Luminex system. Three cytokines (IL-1beta, GM-CSF and IL-13) gave little to no response under all conditions, while six cytokines (TNF-alpha, IL-6, MIP-1alpha, MCP-1, VEGF, and IL-1ra) were clearly detectable. Expression levels generally increased with culture time, particle concentration, and LPS stimulation. Most significantly, it was found that cells treated by Ti discs produced in many instances a higher cytokine expression than did particles.

Kim, M., Wang, C., Benedetti, F., Rabbi, M., Bennett, V., & Marszalek, P. E. (2011). Nanomechanics of Streptavidin Hubs for Molecular Materials. ADVANCED MATERIALS, 23(47), 5684-+.