I am a Biological Chemistry graduate student working in the Dedon Lab in the department of Biological Engineering at MIT. Thanks for visiting my webpage!
2014 - to date, PhD in Biological Chemistry, Massachusetts Institute of Technology, USA
2011 - 2014, Research associate, Process Technical Development, Genentech, South San Francisco, USA
2009 - 2011, PDRP associate, Process Development Rotational Program, Genentech, South San Francisco, USA
2005 - 2009, BS in Chemical Biology, University of California at Berkeley, USA
MIT Department of Chemistry Award for Outstanding Teaching (2014-2015)
Departmental recognition and monetary award given based on teaching evaluations from students
Poster Award, California Separation Science Society (CASSS) Mass Spectrometry Conference (2013)
Poster Title: “Relative Quantitation of Isomerization & Oxidation in a MAb Using a UHPLC-MS-based Assay”
Genentech Protein Analytical Chemistry Departmental Award (2013)
Awarded by senior departmental leadership
Genentech Recognition Award for Contribution to Project/Process (2012)
Genentech Recognition Award for Outstanding Teamwork (2012)
Genentech Process R&D Outstanding Student Award & Scholarship (2008)
Monetary award and summer internship opportunity
Honors, College of Chemistry, UC Berkeley (2006-2009)
My thesis research seeks to define molecular mechanisms that contribute to phenotypic drug resistance in Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis disease (TB). Mtb is responsible for ~2 million deaths each year and latently infects nearly a third of the world’s population. An unusual feature of TB disease is that the infecting bacteria enter a dormant, non-replicative state that can last for years and causes the bacteria to become highly resistant to antibiotics. This drug resistance is termed phenotypic resistance since it involves a normal physiological adaptation and is not due to the acquisition of genomic mutations or resistance plasmids.
The aims of my thesis research are two-fold. First, I propose to test a novel hypothesis that dormancy-induced up-regulation of drug metabolizing enzymes contributes to the antibiotic resistance. Second, I plan to examine whether translational control plays a role in dormancy-induced metabolic remodeling. Moreover, I’d like to exploit this system by developing therapeutics that hinder the bacteria’s physiological adaptation to environmental stress and, ultimately, prevent the emergence of phenotypic antibiotic resistance.