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The University of Southampton
Biological Sciences

Research project: The role of factor inhibiting HIF (FIH) in the development of idiopathic pulmonary fibrosis (IPF)

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FIH is an asparaginyl hydroxylase for HIFα and many ankyrin repeat domain (ARD) containing proteins. The aim of this project is to understand how FIH regulates EMT and its implications in the development of IPF using integrated biochemical, transcriptomic, proteomic and imaging techniques.

Idiopathic pulmonary fibrosis (IPF) is a life threatening condition of the lungs where tissue becomes thickened, stiff, and scarred of unknown cause. The lungs lose their ability to take in and transfer oxygen into the bloodstream. There is a clear unmet clinical need to understand mechanisms of disease in order to improve therapy options. Epithelial-mesenchymal transition (EMT) is crucial during normal embryonic development and is strongly implicated in the pathogenesis of IPF. EMT is a process in which epithelial cells, which line the internal surface of the lung, change into mesenchymal cells, which can deposit scar tissue, one hallmark of IPF.

By 'silencing' genes, one by one, from cells before they undergo EMT as a result of activating a key regulatory gene called RAS, I have screened a number of different proteins that might be controlling this process. I identified a protein called FIH as an important factor, whose reduction prevents this EMT process. It is unlikely that FIH acts alone, and so my next step is to identify which other proteins FIH binds to inside cells – thereby influencing their function in turn.

Together, this will not only illuminate how FIH works but also will define it as a drug target or biomarker to intervene or predict the progression of IPF.

Funding: The Academy of Medical Sciences Springboard/Wellcome Trust
Funding Duration: 2nd October 20017-1st October 2017

Related research groups

Biomedical Sciences
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