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Yi-Ching Lee｜logo Institute of Cellular and Organismic Biology, Academia Sinica

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    Yi-Ching Lee Professor Yi-Ching Lee Research ID Professor Yi-Ching Lee ORCID
    Associate Research Fellow
    • SpecialtyHuman Genetic Diseases, Developmental Biology
    • E-mailyiching@gate.sinica.edu.tw
    • Tel02-2787-1550
    • Website Yi-Ching Lee's Lab
    • LabR502/ICOB
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Professional ExperienceOpenClose
2021
Associate Research Fellow, Institute of Cellular and Organismic Biology, Academia Sinica, Taiwan
2013-2021
Assistant Research Fellow, Institute of Cellular and Organismic Biology, Academia Sinica, Taiwan
2011-2013
Assistant Professor, Institute of Molecular Medicine, National Tsing Hua University, Hsinchu, Taiwan
2009-2011
Adjunct Assistant Professor, Institute of Integrated Medicine, China Medial University, Taichung, Taiwan
2006-2011
Postdoctoral Research Fellow and Group leader, National Center for Genome Medicine, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
2003-2006
Visiting Fellow, National Institute of Child Health& Human Development (NICHD), National Institutes of Health (NIH), Bethesda, MD.
2003
Ph.D., Graduate Institute of Life Science, National Defense University, Taipei, Taiwan
Research InterestOpenClose

The development and progression of complex diseases and even rare diseases are caused by complex interactions between genetic and environmental (including dietary and lifestyle) factors. We aim to delineate the genetic and environmental factors and their interactions contributing to increased risk and progression of genetic diseases. Understanding the pathogenesis and the interplay between gene and environment interactions of complex disease are important steps for personalized medicine and for developing optimal approaches for preventing or delaying the onset of such disorders.

Studying gene-environment interactions of genetic diseases using family- and population-based designs remains extremely challenging. We tackle the challenge starting from characterization of disease-causing genes and pathogenic pathways of rare diseases, followed by stratification of environmental modifiers of the pathogenesis pathways and their effects on disease progression. 

We currently focus on connective tissue disorders, as many common age-related diseases are highly associated with connective tissue deterioration. These diseases include cardiovascular diseases, type II diabetes, bone and cartilage degeneration, and cancers. Furthermore, both genetic and environmental factors play important roles in disease progression. 

Selected PublicationOpenClose
  1. Lin YW, Kao HJ, Chen WT, Kao CF, Wu JY, Chen YT, Lee YC (2023) Cell-based screen identifies porphyrins as FGFR3 activity inhibitors with therapeutic potential for achondroplasia and cancer. JCI Insight 8 (22). doi:10.1172/jci.insight.171257
  2. Jiang CL, Tsao CY, Lee YC (2022) Vitamin C attenuates predisposition to high-fat diet-induced metabolic dysregulation in GLUT10-deficient mouse model. Genes Nutr 17 (1):10. doi:10.1186/s12263-022-00713-y
  3. Wagner BM, Robinson JW, Lin YW, Lee, Y.C., Kaci N, Legeai-Mallet L, Potter LR, 2021, “Prevention of guanylyl cyclase-B dephosphorylation rescues achondroplastic dwarfism.”, JCI insight, 6(9), e147832. 
  4. Jiang, C.L., Jen, W.P., Tsao, C.Y., Chang, L.C., Chen, C.H., Lee, Y.C.* (2020) Glucose Transporter 10 Modulates Adipogenesis via Ascorbic Acid-Mediated Pathway to Protect Mice Against Diet-Induced Metabolic Dysregulation., PLOS Genetics, 16, e1008823. 
  5. Jen, W.P., Chen, H.M., Lin, Y.S., Chern, Y. and Lee, Y.C.* (2020) Twist1 Plays an Anti-apoptotic Role in Mutant Huntingtin Expression Striatal Progenitor Cells. Mol Neurobiol, 57, 1688-1703. 
  6. Syu, Y.W., Lai, H.W., Jiang, C.L., Tsai, H.Y., Lin, C.C. and Lee, Y.C.* (2018) GLUT10 maintains the integrity of major arteries through regulation of redox homeostasis and mitochondrial function. Hum Mol Genet, 27, 307-321. 
  7. Lee, Y.C.,* Song, I.W., Pai, Y.J., Chen, S.D. and Chen, Y.T.* (2017) Knock-in human FGFR3 achondroplasia mutation as a mouse model for human skeletal dysplasia. Sci Rep, 7, 43220. 
  8. Ko, T.M., Kuo, H.C., Chang, J.S., Chen, S.P., Liu, Y.M., Chen, H.W., Tsai, F.J., Lee, Y.C., Chen, C.H., Wu, J.Y.* Chen, Y.T.* (2015) CXCL10/IP-10 is a biomarker and mediator for Kawasaki disease. Circ Res, 116, 876-883. 
  9. Chen, C.H., Lee, C.S., Lee, M.T., Ouyang, W.C., Chen, C.C., Chong, M.Y., Wu, J.Y., Tan, H.K., Lee, Y.C., et al., Chen YT*, Cheng AT* (2014) Variant GADL1 and response to lithium therapy in bipolar I disorder. N Engl J Med, 370, 119-128. 
  10. Lee, Y.C., Kuo, H.C., Chang, J.S., Chang, L.Y., Huang, L.M., Chen, M.R., Liang, C.D., Chi, H., Huang, F.Y., Lee, M.L., Huang, Y.C., Hwang, B., Chiu, N.C., Hwang, K.P., Lee, P.C., Chang, L.C., Liu, Y.M., Chen, Y.J., Chen, C.H., Chen, Y.T.*, Tsai, F.J.*, Wu, J.Y.* (2012) Two new susceptibility loci for Kawasaki disease identified through genome-wide association analysis. Nat Genet, 44, 522-525. 
  11. Khor, C.C.,  Davila, S.,  Breunis, W.B.,  Lee, Y.C.,  Shimizu, C., Wright, V.J., Yeung, R.S., Tan, D.E., Sim, K.S., Wang, J.J. Wong, T.Y.* (2011) Genome-wide association study identifies FCGR2A as a susceptibility locus for Kawasaki disease. Nat Genet, 43, 1241-1246. 
  12. Lee, Y.C., Huang, H.Y., Chang, C.J., Cheng, C.H. and Chen, Y.T.* (2010) Mitochondrial GLUT10 facilitates dehydroascorbic acid import and protects cells against oxidative stress: mechanistic insight into arterial tortuosity syndrome. Hum Mol Genet, 19, 3721-3733.