School of Medicine
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Postdoctoral Research Fellow, Ophthalmology
Current Research and Scholarly Interests Many types of blindness result from the neurons of the retina no longer being able to communicate with the brain due to injury or disease. In mammals, the adult retina cannot make new retinal ganglion cells (the neurons that connect the retina with the brain) to replace those that are lost. In my work, I aim to learn about normal development of retinal ganglion cells and, further, to regenerate new retinal ganglion cells if they are lost in adulthood.
Chien Ting Wu
Postdoctoral Research Fellow, Microbiology and Immunology
Bio 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. As a researcher, I hope to continue my research on the cilium field to help develop better clinical treatments for these patients.
For this reason, I decided to join the Tang Tang Lab in Academia Sinica for my PhD training. The Tang Lab has a longstanding interest in understanding the mechanisms of centriole duplication and is at the forefront of research in the primary cilium field. In this period, I found that Myosin-Va, a motor protein, is required for preciliary vesicle trafficking during the early stage of ciliogenesis. This research was published in Nature Cell Biology.
Thus, my experiences have allowed me to develop my scientific interests and to realize that I would one day like to run my own laboratory and research program focusing on cilium-related diseases.