I started conducting research as a second-year student in college. I entered a biochemical lab to perform research and had my own project. My topic was Alzheimer's disease, and I focused on the relationship between aggregated amyloid-beta and reactive oxygen species levels in cells. I am very grateful for this particular research experience because it allowed me to realize that I am particularly interested in studying disease-associated proteins on a molecular level. Thus, these early research experiences have been invaluable in shaping my scientific interests and personality.
I decided to pursue my graduate training straight out of college by obtaining my master’s degree. I then decided to join the Chen, I-T. Lab for my graduate research training, where I discovered that a novel recombinant protein, LZ8 cloned from Ganoderma, can inhibit the duplication of cancer cells in vitro and decrease the growth rate of tumors in vivo through regulating the p53/MDM2/mTOR signaling pathway. My findings were published in the journal Carcinogenesis. This was my first first-author paper. During this time, I learned how to become an independent scientist.
After my master’s degree, I spent three years completing my military service as a research assistant in Academia Sinica. I worked under the supervision of Prof. Tang Tang. My research focused on the molecular mechanism of centriole duplication. In my research, I found that CEP120, a ciliopathy protein, is required to promote centriole elongation. Overexpression of CEP120 can induce overly long centrioles. This work was published in the Journal of Cell Biology. This was my second first-author paper. Because of these valuable lab experiences, I began to be fascinated by the centriole and cilium field.
Afterwards, to better understand centriole- and cilia-related human hereditary diseases, I worked as a molecular diagnostician in a molecular diagnosis lab at Oregon Health Science University. I used next-generation sequencing (NGS) to identify gene mutations from ciliopathy patients. During this period, I learned how to run a complete molecular diagnosis, draw blood for running NGS, analyzing patient data, preparing patient reports and designing a novel disease panel to run NGS. This experience provided me with a new perspective and connected the things that I learned in the centriole and cilia field, from biochemistry to molecular biology to clinical diagnosis. Most importantly, this experience allowed me to realize that so many people suffer from ciliopathy disease.
I am currently a Postdoctoral Scholar with Dr. Peter Jackson in the Department of Microbiology and Immunology at Stanford University and collaborate with Dr. Raul Andino in the Department of Microbiology and Immunology at University of California, San Francisco. I study the molecular mechanism of respiratory virus infections, including respiratory syncytial virus (RSV), parainfluenza virus (PIV), and SARS-CoV-2, in the human airway epithelium using cell biological and proteomics approaches to identify potential targets for antiviral drug development.
Member, Maternal & Child Health Research Institute (MCHRI)
Honors & Awards
Travel award, 2017 EMBO CONFERENCE-Centrosomes and Spindle Pole Bodies, EMBL Heidelberg, Germany (2017)
Peter Jackson, Postdoctoral Faculty Sponsor
ACE2 localizes to the respiratory cilia and is not increased by ACE inhibitors or ARBs.
2020; 11 (1): 5453
The coronavirus SARS-CoV-2 is the causative agent of the ongoing severe acute respiratory disease pandemic COVID-19. Tissue and cellular tropism is one key to understanding the pathogenesis of SARS-CoV-2. We investigate the expression and subcellular localization of the SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE2), within the upper (nasal) and lower (pulmonary) respiratory tracts of human donors using a diverse panel of banked tissues. Here, we report our discovery that the ACE2 receptor protein robustly localizes within the motile cilia of airway epithelial cells, which likely represents the initial or early subcellular site of SARS-CoV-2 viral entry during host respiratory transmission. We further determine whether ciliary ACE2 expression in the upper airway is influenced by patient demographics, clinical characteristics, comorbidities, or medication use, and show the first mechanistic evidence that the use of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARBs) does not increase susceptibility to SARS-CoV-2 infection through enhancing the expression of ciliary ACE2 receptor. These findings are crucial to our understanding of the transmission of SARS-CoV-2 for prevention and control of this virulent pathogen.
View details for DOI 10.1038/s41467-020-19145-6
View details for PubMedID 33116139