Min Jae Lee

Professor

Seoul National University

Short Biography

Dr. Min Jae Lee is a Professor of Biochemistry at Seoul National University College of Medicine. He earned his Ph.D. from the University of Pittsburgh School of Pharmacy and received postdoctoral training at Harvard Medical School. His research focuses on intracellular protein degradation via the ubiquitin-proteasome system and autophagy, exploring their pathological roles and therapeutic potential. In particular, his work centers on the homeostatic regulation of the proteasome, which is implicated in cancer and neurodegenerative disorders. For example, his laboratory is engineering mammalian 26S proteasomes to utilize them as direct, targeted protein degraders—a project supported by Samsung Electronics. Additionally, he investigates the aggregation mechanism of tau protein to uncover novel therapeutic strategies for Alzheimer’s disease. Dr. Lee has authored over 70 research articles, including 13 publications with more than 100 citations, accumulating over 5,500 citations in total. He has received numerous honors, including the Research Excellence Prize from the Korean Chemical Society, the Young Scientist Award, and the Sasuk Award from the Korean Society for Biochemistry and Molecular Biology.

Presentation Topic: Directly engaging 26S Proteasomes for Ubiquitin-Independent Target Degradation 
• We developed Prote-a-Tac, a targeted protein degradation (TPD) strategy that directly engages the 26S proteasome, bypassing the need for Ub ligase-mediated polyubiquitination.
• Prote-a-Tac is a heterobifunctional chimera combining a proteasome-binding module with a target-specific antibody, enabling selective degradation of overexpressed and endogenous proteins.
• The platform is highly modular and specific, allowing flexible target switching and demonstrated high specificity validated by quantitative mass spectrometry.
• mRNA-based lipid nanoparticle delivery of Prote-a-Tac in cells and mouse xenograft models resulted in effective target degradation and delayed tumor progression.