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Research Associate/Fellow (Fixed term)

University of Nottingham - Life Sciences

Location: Nottingham
Salary: £32,080 to £35,608 per annum, depending on skills and experience (£35,608 with relevant PhD)
Hours: Full Time
Contract Type: Fixed-Term/Contract
Placed On: 7th April 2026
Closes: 24th April 2026
Job Ref: MED263526

This role will provide support to an ongoing MRC project grant characterising the molecular pharmacology of the P2Y2 receptor (P2Y2R).  The P2Y2R is a Class A GPCR physiologically activated by the nucleotides UTP and ATP. Subsequent Gq mediated signalling ultimately drives inflammation, wound healing and cell migration. Aberrant P2Y2R mediated signalling has been implicated in pathological inflammation and fibrosis in progressive diseases such as idiopathic pulmonary fibrosis (IPF) and cancer growth and metastasis. Therapeutic strategies aimed at modulating P2Y2R activity would therefore have considerable utility as anti-inflammatory or anti-fibrotic treatments. However, drug discovery programmes targeting P2Y2R have had limited success due to the low affinity and/or poor bioavailability of compounds which has been further exacerbated by a lack of detailed P2Y2R specific structural information and pharmacological characterisation.  

We have recently developed novel selective fluorescent antagonists for scientific investigation of the P2Y2R (Conroy et al., 2018 (doi.org/10.1021/acs.jmedchem.8b00139); Knight et al., 2024 (doi.org/10.1021/acsmedchemlett.4c00211)). The role holder will use these novel fluorescent antagonists alongside bioluminescence resonance energy transfer (BRET), confocal imaging and downstream functional assays (calcium mediated signalling assays, G protein recruitment assays) to quantify the molecular pharmacology of the P2Y2R in living cells. Additionally, the role holder will characterise the molecular pharmacology of physiologically relevant P2Y2R alternative transcripts and a series of point mutations of residues implicated in ligand binding, receptor expression and downstream signalling.

Candidates should have a PhD (or close to completion) or equivalent in pharmacology or a related discipline, along with a proven track record of molecular pharmacology research and experience with the study of G protein-coupled receptors in living cells. Experience in resonance energy transfer assays and quantitative downstream signalling assays is also required.

The successful candidate will join a vibrant molecular pharmacology focused research group embedded within the Centre of Membrane Proteins and Receptors (COMPARE) at the University of Nottingham. COMPARE is a joint initiative between the Universities of Nottingham and Birmingham using imaging to study membrane bound receptors www.birmingham-nottingham.ac.uk/compare.

This is a full-time (36.25 hours), fixed-term post for 6 months from 1st July 2026. Requests for secondment from internal candidates will be considered on the basis that prior agreement has been sought from both your current line manager and the manager of your substantive post, if you are already undertaking a secondment role.

Informal enquiries may be addressed to Professor Stephen Hill: steve.hill@nottingham.ac.uk or Dr Laura Kilpatrick: laura.kilpatrick@nottingham.ac.uk. Please note that applications sent directly to these Email addresses will not be accepted.

The School of Life Sciences holds an Athena Gold SWAN Award, in recognition of our commitment to supporting and advancing women’s careers in the life sciences (STEMM). 

Further details:

We are the first university to have achieved Athena Swan Gold Award.

To help you succeed, we published Candidate Guidance to provide support on the application and interview process.

Discover our benefits, visit Your Benefits website.

We welcome applications from UK, Europe and worldwide and aim to make your move to the UK as smooth as possible. Visit the Moving to Nottingham page for details.

Your application will be considered on an equal basis, subject to the relevant permission to work in the UK as set out by UK Visas & Immigration.

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