Inflammatory bowel disease (IBD) is characterised by chronic inflammation of the Gastrointestinal (GI) tract. Studies have shown activation of hypoxia-inducible pathways can promote the resolution of inflammatory disease. This occurs, in part, through regulation of autophagy and endoplasmic reticulum (ER)-stress/unfolded protein response (UPR) pathways, and potentially, their co-ordinated action. Not surprisingly, there is considerable interest in harnessing hypoxia-inducible pathways for potential IBD therapies; however this can only be achieved once we fully understand the biological mechanisms.
This clinically-relevant project would look to examine the functional effects of hypoxia on IBD using an in vitro model of IBD and a range of techniques, including mammalian cell culture, immunoblotting and qPCR, confocal microscopy and immunohistochemistry. In particular, it would focus on the importance of UPR and autophagic pathways and how they functionally intersect to resolve hypoxia-induced inflammation in IBD. This model and the research data generated from its will ultimately advance our understanding of the cellular and molecular mechanisms contributing to IBD.
A first degree (at least a 2.1) ideally in biomedical sciences or equivalent discipline with a good fundamental knowledge of cell biology and molecular biology associated techniques.
IELTS score must be at least 6.5 (with not less than 6.0 in each of the four components). Other, equivalent qualifications will be accepted. Full details of the University’s policy are available online.
• Experience of fundamental GLP, record keeping, troubleshooting, data handling and presentation skills
• Competent in basic laboratory skills
• Knowledge of cell biology and analytical techniques
• Good written and oral communication skills
• Strong motivation, with evidence of independent research skills relevant to the project
• Good time management
Prior laboratory experience in mammalian cell culture and molecular biology is desirable