Laboratory of Jin Mo Park, PhD

Overview

Research in the Park laboratory revolves around the question, “How do environmental and endogenous physiological changes reprogram genetically hard-wired molecular pathways directing cell fate and function?” Park and his colleagues address this question by investigating signaling and gene regulatory events in immune disorders and cancer. The goal of this research is to determine the molecular underpinnings of human diseases and devise clinical strategies for their prevention and treatment. The major experimental approaches used in the Park laboratory involve genetic and pharmacological tools for the perturbation of molecular processes in various cell types and biochemical methods for their analysis.

Research Projects

1. Signaling pathways crucial for barrier tissue homeostasis and inflammation
2. Cancer cell fates and host immune responses in the tumor microenvironment
3. Immune sensing and signaling mechanisms in host-microbe interactions

Publications

Complete list of published work

Selected Publications

• Kim, C., Sano, Y., Todorova, K., Carlson, B.A., Arpa, L., Celada, A., Lawrence, T., Otsu, K., Brissette, J.L., Arthur, J.S.C. and Park, J.M. The kinase p38alpha serves cell type-specific inflammatory functions in skin injury and coordinates pro- and anti-inflammatory gene expression. Nat Immunol 2008; 9:1019-1027.
• Enzler, T., Sano, Y., Choo, M.-K., Cottam, H.B., Karin, M., Tsao, H. and Park, J.M. Cell-selective inhibition of NF-kappaB signaling improves therapeutic index in a melanoma chemotherapy model. Cancer Discov 2011; 1:496-507.
• Ritprajak, P., Hayakawa, M., Sano, Y., Otsu, K. and Park, J.M. Cell type-specific targeting dissociates the therapeutic from the adverse effects of protein kinase inhibition in allergic skin disease. Proc Natl Acad Sci U S A 2012; 109:9089-9094.
• Sano, Y. and Park, J.M. Loss of Epidermal p38αlpha signaling prevents ultraviolet radiation-induced inflammation via acute and chronic mechanisms. J Invest Dermatol 2014; 134:2231-2240.
• Caballero-Franco, C., Guma, M., Choo, M.-K., Sano, Y., Enzler, T., Karin, M., Mizoguchi, A. and Park, J.M. Epithelial control of gut-associated lymphoid tissue formation through p38alpha-dependent restraint of NF-kappaB signaling. J Immunol 2016;196: 2368-2376.
• Hayakawa, M., Hayakawa, H., Petrova, T., Ritprajak, P., Sutavani, R.V., Jiménez-Andrade, G.Y., Sano, Y., Choo, M.-K., Seavitt, J., Venigalla, R.K.C., Otsu, K., Georgopoulos, K., Arthur, J.S.C. and Park, J.M. Loss of functionally redundant p38 isoforms in T cells enhances regulatory T cell induction. J Biol Chem 2017; 292: 1762-1772.
• Choo, M.-K., Sano, Y., Kim, C., Yasuda, K., Li, X.-D., Lin, X., Stenzel-Poore, M., Alexopoulou, L., Chen, Z.J., Stewart, G.C., Chong, H. and Park, J.M. TLR sensing of bacterial spore-associated RNA triggers host immune responses with detrimental effects. J Exp Med 2017; 214: 1297-1311.
• Choo, M.-K., Kraft, S., Missero, C. and Park, J.M. The protein kinase p38αlpha destabilizes p63 protein to limit epidermal stem cell frequency and tumorigenic potential. Sci Signal 2018; 11: eaau0727.
• Jiménez-Andrade, Y., Hillette, K.R., Yoshida, T., Kashiwagi, M., Choo, M.-K., Liang, Y., Georgopoulos, K. and Park, J.M. The developmental transcription factor p63 is redeployed to drive allergic skin inflammation through phosphorylation by p38alpha. J Immunol 2022; 208: 2613-2621.