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University of Exeter Medical School

 Professor Sebastian Oltean

Professor Sebastian Oltean

Associate Professor
Clinical and Biomedical Sciences

Medical School Building F.08B
University of Exeter
Medical School Building
St Luke's Campus
Exeter EX1 2LU

About me:

Sebastian studied medicine at “Iuliu Hatieganu” Medical School, Cluj-Napoca, Romania and trained as a junior doctor in Nephrology and Dialysis before moving to USA where he obtained a PhD from the University of Nebraska-Lincoln in 2004.This was followed by postdoctoral training at Duke University Medical Center (North Carolina, USA) where he became interested in studying the connections between alternative splicing and cancer. In 2008 he moved to the University of Bristol where he continued to study alternative splicing in vivo, with focus towards the importance of several genes splice isoforms (e.g VEGF, FGFR2) in cancer as well as kidney diseases and development of splice-based therapeutics. In 2012 he was appointed Independent Research Fellow and Principal Investigator and developed his own research group in Bristol before moving to the University of Exeter Medical School in 2017.


Interests:

The main goals of my research projects are to understand molecular mechanisms of disease and to find novel therapeutic targets. As disease models, I work on diabetes (especially diabetic nephropathy) and cancer (especially prostate cancer). The cellular processes that I am most interested in are angiogenesis, epithelial-mesenchymal transitions and fibrosis. At molecular level I study alternative splicing regulation in physiology and disease, with a special emphasis on how we can manipulate alternative splicing for therapeutic benefit.

 

Alternative splicing is one of the main processes that decide the diversity of proteins in our bodies. It is estimated that ~94% of genes are alternatively spliced in humans and therefore this process affects all cellular properties. The function of the majority of splicing isoforms is not characterized yet. Numerous splicing isoforms have been associated with disease progression in recent years and there is much interest in understanding their contribution to pathogenesis and how this can be reversed for therapeutic purposes.

 

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