Yun is a postdoctoral research scholar in Dr. Anna Gloyn lab (Translational Genomics of Diabetes Lab). Since she joined the lab in August 2022, she has been involved in projects investigating type 2 diabetes (T2D) susceptible genes and their molecular mechanisms for pancreatic beta-cell dysfunction under the mentorship of Dr. Gloyn. In particular, she is interested in how T2D effector transcripts alter the autophagy/mitophagy pathways in human pancreatic beta-cells and how this may lead to beta-cell failure, mitochondrial dysfunction and T2D pathology. She has been also digging into genetic mutations which are a cause of neonatal diabetes using CRISPR genome editing technique in human induced pluripotent stem cell (hiPSC) line. Her role is to generate stem cell model to establish these mutations cause haploinsufficiency.
During her PhD, she focused on the roles of an epigenetic regulator and its molecular machineries in the pathogenesis of non-alcoholic fatty liver disease (NAFLD)/now metabolic dysfunction-associated steatotic liver disease (MASLD). Besides, she studied the correlation between endoplasmic reticulum (ER) stress-mediated unfolded protein response (UPR) signalling and autophagy, and further their effects on various cells using some plant extracts. Her research goal is to expand our knowledge about the cellular and molecular mechanisms of T2D and explore therapeutic targets and/or strategies.

Honors & Awards

  • Finalist for a Poster Award, The 15th Annual Pediatrics Research Retreat 2024 (Apr 2024)
  • Keystone Symposia Scholarship ($1,200), Keystone Symposia & NIH NIDDK (Aug 2022)
  • Best Poster Award, The Korean Society for Integrative Biology Conference (Dec 2021)
  • Keystone Financial Aid-Scholarship Program, Keystone Symposia (June 2021)
  • Brain Korea 21 Scholarship, Brain Korea 21 Program (Mar 2017-Feb 2019)

Stanford Advisors

All Publications

  • Effect of RNF113A deficiency on oxidative stress-induced NRF2 pathway Animal Cells and Systems Cho, N., Kim, Y., Lee, Y., Choi, D., Park, C., Kim, J., Kim, K., Kim, K. 2024; 28 (1): 261-271
  • PAX4 loss of function increases diabetes risk by altering human pancreatic endocrine cell development. Nature communications Lau, H. H., Krentz, N. A., Abaitua, F., Perez-Alcantara, M., Chan, J. W., Ajeian, J., Ghosh, S., Lee, Y., Yang, J., Thaman, S., Champon, B., Sun, H., Jha, A., Hoon, S., Tan, N. S., Gardner, D. S., Kao, S. L., Tai, E. S., Gloyn, A. L., Teo, A. K. 2023; 14 (1): 6119


    The coding variant (p.Arg192His) in the transcription factor PAX4 is associated with an altered risk for type 2 diabetes (T2D) in East Asian populations. In mice, Pax4 is essential for beta cell formation but its role on human beta cell development and/or function is unknown. Participants carrying the PAX4 p.His192 allele exhibited decreased pancreatic beta cell function compared to homozygotes for the p.192Arg allele in a cross-sectional study in which we carried out an intravenous glucose tolerance test and an oral glucose tolerance test. In a pedigree of a patient with young onset diabetes, several members carry a newly identified p.Tyr186X allele. In the human beta cell model, EndoC-βH1, PAX4 knockdown led to impaired insulin secretion, reduced total insulin content, and altered hormone gene expression. Deletion of PAX4 in human induced pluripotent stem cell (hiPSC)-derived islet-like cells resulted in derepression of alpha cell gene expression. In vitro differentiation of hiPSCs carrying PAX4 p.His192 and p.X186 risk alleles exhibited increased polyhormonal endocrine cell formation and reduced insulin content that can be reversed with gene correction. Together, we demonstrate the role of PAX4 in human endocrine cell development, beta cell function, and its contribution to T2D-risk.

    View details for DOI 10.1038/s41467-023-41860-z

    View details for PubMedID 37777536

    View details for PubMedCentralID 5034897

  • Kazinol C from Broussonetia kazinoki stimulates autophagy via endoplasmic reticulum stress-mediated signaling ANIMAL CELLS AND SYSTEMS Lee, Y., Kwon, J., Jeong, J., Ryu, J., Kim, K. 2022; 26 (1): 28-36


    Autophagy modulators are considered putative therapeutic targets because of the role of autophagy in cancer progression. Kazinol C, a 1,3-diphenylpropane from the plant Broussonetia kazinoki, has been shown to induce apoptosis in colon cancer cells through the activation of AMPK at high concentrations. In the present study, we found that Kazinol C induced autophagy through endoplasmic reticulum stress-mediated unfolded protein response signaling in several normal and cancer cell lines at low concentrations of Kazinol C that did not induce apoptosis. Kazinol C activated the transducers of unfolded protein response signaling, leading to target gene expression, LC3-II conversion, and TFEB nuclear translocation. Chemical inhibition of endoplasmic reticulum stress reduced LC3-II conversion. In addition, blockade of autophagy by knockout of Atg5 or treatment with 3-MA enhanced Kazinol C-induced apoptosis. In summary, we have uncovered Kazinol C as a novel autophagy inducer and confirmed the role of autophagy as a cellular stress protector.

    View details for DOI 10.1080/19768354.2021.2023628

    View details for Web of Science ID 000741205000001

    View details for PubMedID 35308126

    View details for PubMedCentralID PMC8928802

  • Inhibition of autophagy sensitizes lignan-induced endoplasmic reticulum stress-mediated cell death BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS Kwon, J., Lee, Y., Jeong, J., Ryu, J., Kim, K. 2020; 526 (2): 300-305


    Relationship between autophagy and endoplasmic reticulum (ER) stress and their application to treat cancer have been actively studied these days. Recently, a lignan [(-)-(2R, 3R)-1,4-O-diferuloylsecoisolariciresinol, DFS] from Alnus japonica has been found to reduce the viability of colon cancer cells. In this study, we have observed DFS-induced autophagy in a variety of cancer cell lines. In addition, DFS led to ER stress, based on the activation of unfolded protein response (UPR) transducers and an elevated expression of UPR target genes in prostate and colon cancer cells. Further investigation has shown that DFS triggered the activation of AMP-activated protein kinase (AMPK) signaling and nuclear translocation of transcription factor EB (TFEB). Furthermore, the cytotoxicity of DFS was potentiated by the co-treatment of autophagy inhibitor in these cancer cells. This study has provided a noble implication that the combination of DFS and autophagy inhibition exerts a synergistic effect in cancer treatment.

    View details for DOI 10.1016/j.bbrc.2020.03.081

    View details for Web of Science ID 000530031800004

    View details for PubMedID 32209256