Ester completed an undergraduate degree at the University of St. Andrews in Biomolecular Sciences (Honours) where her dissertation project focused on the cloning of proteins thought to be implicated in Alzheimer's Disease. She went on to do a Masters in Biomedical Sciences at St. Georges University of London, studying the development of Paediatric Germ Cell Tumours as a consequence of errant Hedgehog Signalling. In addition, she has carried out several internships at both Johns Hopkins University in Baltimore, USA and Harvard Medical School where the aim was to map the peripheral nervous system.
My research project is looking at the relationship between cAMP signalling and Polycystin function, particularly in the scope of Polycystic Kidney Disease. Autosomal Dominant Polycystic Kindey Disease (ADPKD) is the fourth most common cause of end-stage renal disease and it is characterised by progressive enlargement of cysts in the kidneys, liver cysts, cardiac failure, and intracranial aneurysms. Thus far there is no cure for PKD as the underlying mechanism involved in disease progression is still not fully understood. ADPKD is known as a “ciliopathy”, a disease that arises from a genetic mutation in proteins of the primary cilium, an organelle which is vital for cell signalling and organ development. Two genes are responsible for ADPKD, PKD1 and PKD2, which code for two ciliary proteins known as Polycystin 1 (PC1) and 2 (PC2) respectively. It is believed the two transmembrane proteins PC1 and PC2 interact with the cAMP signaling pathway, a tightly regulated cascade, responsible for a plethora of intracellular responses including cell proliferation and apoptosis. cAMP signaling is upregulated in ADPKD cystic cells, and it is hypothesized PC1 and PC2 interactions with cAMP at different subcellular locations may drive ADPKD progression. Shedding light on the PC1/2 and cAMP interplay at subcellular domains, such as the primary cilium, could help us elucidate new therapeutic targets for ADPKD.