Nicholas M Levinson

Nicholas M Levinson is an Associate Professor in the Department of Pharmacology at the University of Minnesota, specializing in cellular mechanisms of cancer. His research focuses on kinase biochemistry and the development of novel cancer therapeutics with emphasis on Aurora kinase A and RAF signaling pathways.

Dr. Levinson's research interests center on kinase signaling pathways in cancer development and progression. His work explores:

• Mechanisms of Aurora kinase A in cancer
• Allosteric regulation of protein kinases
• Development of kinase inhibitors and degraders
• Signal transduction in neuroblastoma and MYC-driven cancers
• Protein conformational dynamics in kinase activation
• Novel drug discovery platforms for allosteric inhibitors

Analysis of Dr. Levinson's publication record (26 total outputs from 2006-2025) reveals an increasing focus on translational cancer research, particularly targeting kinase signaling pathways. His recent work (2023-2025) demonstrates sophisticated approaches to understanding kinase allostery and developing next-generation therapeutics including degraders and allosteric inhibitors for challenging cancer targets.

Dr. Levinson has secured significant research funding as Principal Investigator:

• Allosteric mechanisms driving paradoxical activation of RAF kinases (NIH, 2024-2026)
• Targeting allosteric scaffolding functions of Aurora kinase A in cancer (NCI, 2021-2026)
• A transformative drug discovery platform for allosteric kinase inhibitors (NCI, 2021-2026)
• Time-resolved FRET-based allostery sensors for protein kinase drug targets (NCI, 2020-2024)
• Targeting N-Myc with selective Aurora kinase A degraders for neuroblastoma therapy (DoD, 2021-2025)

His laboratory employs advanced biophysical techniques including time-resolved FRET to study protein conformational dynamics, structural biology approaches, and translational models to investigate kinase signaling in cancer and develop therapeutic strategies with particular focus on neuroblastoma and other MYC-driven cancers.