Research Associate in Idiopathic Pulmonary Fibrosis

Closing Date : 02/07/2017
Employment Type : Fixed Term
Duration : 1 July 2017 until 30 June 2019 with the possibility of a further year
Faculty / Organisational Unit : Biology, Medicine & Health
School/Directorate : School of Biological Sciences
Division : -
Hours Per week : Full time
Salary : £31,076 to £38,183 per annum according to relevant experience.
Location : Oxford Road, Manchester
Job Reference : BM&H-10158

The research centre has established a new research initiative in fibrosis. The initiative is based on recent discoveries in the Centre, which provide a platform for novel approaches to the problem. Fibrosis is a complex process and contributes massively to all major chronic diseases, such as those affecting the kidney, liver, heart, lung and intestine. Our plan is thus for a new approach aimed at tackling the fundamental mechanisms that underpin fibrosis.  Supported by generous funds, and building on the collaborative culture and excellence in training and technology development in the Centre, our goals are to elucidate pioneering concepts in cell-matrix research, and use these understand the basis of fibrosis.

To spearhead this initiative we are funding four pilot projects, each driven by a postdoctoral associate. These posts are funded for 2 years, in the first instance, with the possibility for a third year of funding. Each project is expected to attract external funding after the initial pilot phase.  The project titles are:

1)     The role of pro-fibrotic cytokines in the regulation of collagen turnover.

2)     The circadian clock in goblet cells as a gate-keeper for mucosal matrix production.

3)     Elucidating the high-resolution structures of cell-matrix assemblies using cryo electron microscopy.

4)     Identification of the cellular reprogramming pathways that convert healthy cells to a fibrotic phenotype in idiopathic pulmonary fibrosis.

These projects build on the Centre’s recent discoveries in circadian clock regulation of matrix synthesis, the mechanical sensing of the matrix by cells, the role of pro-fibrotic stimuli from immune cells to perturb matrix homeostasis and the recognition of the key role of supramolecular structures in defining matrix assembly.

Matrix (‘extracellullar matrix’) is essential for multicellular life. Matrix stress shields cells from environmental forces and provides a dynamic scaffold for cell attachment, migration, differentiation and fate specification. Thus, mechanisms that maintain healthy matrix structure and organisation are essential to ensure the appropriate size, shape, and mechanical properties of tissues needed to support their specialized functions. However, the accumulation of excess, or inappropriate matrix, as occurs in fibrosis, can cause the loss of tissue/organ function and lead to death. Our vision is that understanding the physical, chemical, and temporal crosstalk between cells and matrix will generate profound insights into the mechanisms that underpin tissue assembly and function, and enable us to identify why the dysregulation of matrix causes fibrosis, which is a major factor in many chronic diseases. Our strategy is aimed at the fundamental biology driving the development of fibrosis as we feel this will identify novel routes for disease intervention.

Successful candidates will be subject to pre-employment screening carried out on our behalf by a third party. The offer of employment will be dependent on the successful candidate passing that screening. Whilst you will be required to provide express consent at a later stage, by continuing with your application now you acknowledge that you are aware that such screening will take place, and agree to take part in the process.

Please note that we are unable to respond to enquiries, accept CVs or applications from Recruitment Agencies.

General enquiries:

Email: hrservices@manchester.ac.uk

Tel: 0161 275 4499

Technical support:

Email: universityofmanchester@helpmeapply.co.uk

Tel: 01565 818 234

This vacancy will close for applications at midnight on the closing date.

Further Particulars:

 

This position is now closed. We are no longer accepting applications for this position.