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Wong, Esther

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Wong, Esther

Wong, Siew Peng Esther
Assistant Professor

Office: 03n-05
Telephone: 6316 2848
Email: EstherWong@ntu.edu.sg

 

Education

  • BSc (Hons)- Microbiology, National University of Singapore (1998)
  • PhD- Microbiology, National University of Singapore (2004)

Professional Experience

  • Postdoctoral Fellow, National Neuroscience Institute, Singapore (2004)
  • Research Fellow, Albert Einstein College of Medicine, NY, USA (2007)
  • Instructor, Albert Einstein College of Medicine, NY, USA (2010)
  • Assistant Professor, School of Biological Sciences, NTU, Singapore (2011)

Research Interest

All cells are endowed with a variety of surveillance systems that detect unwanted or damaged proteins and eliminate them before they become toxic to the cells. One of which is autophagy which is a “self-eating” mechanism used by cells to degrade proteins in lysosomes. My laboratory is interested to elucidate yet unknown mechanisms in the degradation of proteins by autophagy and how the related defects result in accumulation of damaged components, proteotoxicity and loss of cognitive functions associated with neurodegeneration and aging.

Fig. 1. Three forms of autophagy in mammalian cells.

Fig. 1. Three forms of autophagy in mammalian cells.

Three forms of autophagy have been described in mammalian cells: macroautophagy (MA), microautophagy (MI) and chaperone-mediated autophagy (CMA) (Fig. 1). Harnessing autophagy to control protein homeostasis has been shown to be protective in many age-related pathologies. Central to my research focus is the characterization of the mechanisms behind autophagic dysfunction in neurodegeneration. We have identified defects in CMA and MA that compromise the quality control functions of these autophagic pathways leading to pathogenesis in numerous neurodegenerative diseases including Parkinson’s disease (PD), Huntington’s disease (HD), Alzheimer’s disease and tauopathies. Understanding the mechanisms underlying these aberrations will allow us in future delineating interventions to restore autophagic function and prevent or slow down the progression of these severe disorders. In addition, autophagic activity also decreases with physiological aging resulting in the progressive intracellular accumulation of nonfunctional proteins characteristic of old organisms. In particular, prevention of the age-related decline in CMA has been shown to preserve “young-like” cellular and organ function as well as homeostasis in mice. These major beneficial effects underscore the importance of determining new means to regulate/restore the activities of different autophagic pathways. Our recent work supports a novel connection between ubiquitination and autophagy. The other goal of my research is to elucidate the regulatory role of the ubiquitin system over certain selective forms of autophagy and understand how changes in this regulatory mechanism with age contribute to autophagic dysfunction in aging and age-related disorders.