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Natasha Ng

DPhil student

Research overview

Natasha joined the Gloyn group in 2012 as a DPhil student and is currently supervised by both Professors Anna Gloyn and Patrik Rorsman. Her graduate degree is funded by a research scholarship from A*STAR in Singapore, who also provided for her undergraduate studies in Biology at Imperial College London. Upon graduation she spent a year as a research assistant back at A*STAR, where she contributed to the study of how host factors regulate Hepatitis B virus replication in the context of hepatocellular carcinoma. She then moved into the field of diabetes and metabolism at Oxford and is affiliated with Balliol College.

Natasha is interested in understanding the effects of genetic variants that have been linked to diabetes and related glycemic traits at the level of the molecule, the cell and the whole organism. Functional investigation of rare variants identified through exome studies can shed light on the mechanisms that may drive the association and that potentially influence disease risk.  Her thesis research focuses on characterising variants in G6PC2 and more fundamentally understanding the role of G6PC2 in the pancreatic beta cells, using a combination of molecular biology, cellular assays and imaging tools. Her work will add to the biological knowledge of how G6PC2 function affects glucose homeostasis.

Outside of work she is an avid volunteer with the University of Oxford museums and the teaching charity Jacari. In her free time, Natasha wishes she could be a graphic designer or graffiti artist. Perhaps some time in future she would merge her interests in medical science, graphic design and public engagement.

Selected publications

Mahajan A , Sim X, Ng HJ, Manning A, Rivas M, Highland H et al Identification and functional characterization of G6PC2 coding variants Influencing glycemic traits define an effector transcript at the G6PC2-ABCB11 locus. PLoS Genetics 2015 Jan 27;11(1):e1004876. doi: 10.1371/journal.pgen.1004876. eCollection 2015.

Ng HJ & Gloyn AL. Bridging the gap between genetic associations and molecular mechanisms for type 2 diabetes. Current Diabetes Reports 2013;13:778-85.

Ko  HL, Ng HJ, Goh EH et al. Reduced ADP-ribosylation by PARP1 natural polymorphism V762A and by PARP1 inhibitors enhance Hepatitis B virus replication. Journal of Viral Hepatitis 2013;20:658-65.