Young Mi Oh, PhD
Education
- BS, Life Sciences and Biotechnology, Korea University
- PhD, Biological Science, Seoul National University
- Postdoctoral Study, Developmental Biology & Neuroscience, Washington University School of Medicine
Research Interest
Dr. Oh’s lab focuses on studying the mechanism of disease onset in neurodegenerative diseases through miRNA-mediated neuronal reprogramming that has the potential to yield valuable insights into the underlying causes of these disorders. By generating reprogrammed neurons from patient-derived fibroblasts and investigating the role of miRNA in neuronal subtype generation, Dr. Oh’s lab aims to recapitulate disease pathology while maintaining age and disease-related characteristics. This approach could provide a valuable platform for understanding why neurodegenerative diseases manifest pathology later in life and identifying the factors that drive the onset of these diseases.
Selected Publications
- Oh YM*, Lee SW* (2024). Patient-derived neuron model: Capturing age-dependent adult-onset degenerative pathology in Huntington’s disease. Molecules and Cells, 47(4): 100046. *co-corresponding authors.
- Oh YM*, Lee SW*, Yoo AS (2024). Striatal neuronal models of Huntington’s disease via direct conversion: Modeling age-dependent disease phenotypes. Huntington’s Disease, 17;411-426. *co-first authors.
- Lee SW*, Oh YM*, Victor MB, Yang Y, Chen S, Strunilin I, Dahiya S, Dolle RE, Pak SC, Siverman GA, Perlmutter DH, Yoo AS. (2024). Longitudinal modeling of human neuronal aging reveals the contribution of the RCAN1–TFEB pathway to Huntington’s disease neurodegeneration. Nature Aging, 4;95-109. *co-first authors.
- Oh YM*, Lee SW*, Yoo AS. (2023). Modeling Huntington disease through microRNA-mediated neuronal reprogramming identifies age-associated autophagy dysfunction driving the onset of neurodegeneration. Autophagy, 8;1-3. *co-first authors.
- Oh YM*, Lee SW*, Kim WK, Chen S, Church VA, Cates K, Li T, Zhang B, Dolle RE, Dahiya S, Pak SC, Silverman GA, Perlmutter DH, Yoo AS. (2022). Age-associated decline in autophagy mediated by mir-29b-3p plays a key role in neurodegeneration in Huntington’s disease patient-derived neurons. Nature Neuroscience, 25(11):1420-1433. *co-first authors.
- Deng PY, Carlin D, Oh YM, Myrick LK, Warren ST, Cavalli V, Klyachko VA. (2019). Voltage-Independent SK-Channel Dysfunction Causes Neuronal Hyperexcitability in the Hippocampus of Fmr1 Knock-Out Mice. J Neurosci., 39(1):28-43.
- Oh YM*, Mahar M*, Ewan EE, Leahy KM, Zhao G, Cavalli V. (2018). Epigenetic regulator UHRF1 inactivates REST and growth suppressor gene expression via DNA methylation to promote axon regeneration. Proc Natl Acad Sci U S A., 115(52): E12417-E12426. *co-first authors.
- Lee SW, Oh YM, Lu YL, Kim WK, Yoo AS. (2018). MicroRNAs Overcome Cell Fate Barrier by Reducing EZH2-Controlled REST Stability during Neuronal Conversion of Human Adult Fibroblasts. Dev Cell., 46(1):73-84
- Cho Y, Shin JE, Ewan EE, Oh YM, Pita-Thomas W, Cavalli V. (2015). Activating Injury-Responsive Genes with Hypoxia Enhances Axon Regeneration through Neuronal HIF-1α. Neuron., 88(4):720-34
- Oh YM, Lee SB, Choi J, Suh HY, Shim S, Song YJ, Kim B, Lee JM, Oh SJ, Jeong Y, Cheong KH, Song PH, Kim KA. (2014). USP8 modulates ubiquitination of LRIG1 for Met degradation. Sci Rep., 4:4980.
- Oh YM, Song Y-J, Lee SB, Jung Y, Kim B, Kim GW, Kim KE, Lee JM, Cho M-Y, Choi J, Nam D-H, Song PH, Cheong KH, Kim K-A. (2012). A new anti-c-Met antibody selected by a mechanism-based dual-screening method: therapeutic potential in cancer. Mol. Cells., 34:1-10.
- Oh YM, Kwon YE, Kim JM, Bae SJ, Lee BK, Yoo SJ, Chung CH, Deshaies RJ, Seol JH. (2009). Chfr is linked to tumour metastasis through the downregulation of HDAC1. Nature Cell Biol.,11(3):295-302.
- Oh YM, Yoo SJ, Seol JH. (2007). Deubiquitination of Chfr, a checkpoint protein, by USP7/HAUSP regulates its stability and activity. Biochem Biophys Res Commun., 8;357(3):615-9.
Click here for a full list of Dr. Oh’s publications.