Current Vacancies
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Key details
- Location University of Dundee
- Salary: £37,174 - £42,882 per annum
- Lab: Prof. Miratul Muqit
MRC Protein Phosphorylation and Ubiquitylation Unit (MRC PPU):
The MRC PPU is one of the world's most renowned centres for research on protein phosphorylation and ubiquitylation (http://www.ppu.mrc.ac.uk/). Many world-leading researchers in the field of signal transduction have trained within the MRC PPU. The major aims of the MRC PPU are to advance understanding of the role of protein phosphorylation and ubiquitylation in cell regulation and human disease, to facilitate the development of drugs to treat diseases caused by abnormalities in phosphorylation, to generate reagents and improve technologies. A key remit of the MRC PPU is to train the next generation of scientists who will advance our understanding in this crucial area of medical research.
Division of Signal Transduction Unit (DSTT):
The Division of Signal Transduction Therapy (DSTT) was established in 1998. This division operates as a unique collaboration between scientists in the MRC PPU and signalling researchers at the University of Dundee's School of Life Sciences and the pharmaceutical industry. The DSTT is widely regarded as a model for how academia should interact with industry. The DSTT operates as a simple bridging mechanism to enable our PIs working on ubiquitylation and phosphorylation to effectively interact with major pharmaceutical companies to help accelerate the early stages of drug discovery.
We are recruiting up to three postdoctoral scientists to join the laboratory of Professor Miratul Muqit, with expertise in signalling, cell biology, mouse neurobiology, CRISPR gene-editing or proteomics to investigate the function of the PINK1 kinase in neurons and the brain. The overarching goal of the Muqit lab is to undertake fundamental research to understand the molecular basis of the neurodegenerative disorder, Parkinson's disease (PD), through open and interdisciplinary collaborations with leading research groups across the world.
The successful applicant(s) will undertake discovery-driven research projects as part of a Medical Research Council Programme Grant Award that will lead to better understanding of PD and how to diagnose and treat it. The Muqit Lab is exemplar in collaborative research to make robust discoveries and share data openly in the field to accelerate progress.
The project(s) will investigate mechanisms of the PINK1 kinase which is frequently mutated in early-onset PD and is a master-regulator of mitophagy in brain. Previous research by the Muqit lab has contributed to the development of targeted therapies for PINK1-induced mitophagy which entered clinical trials for PD patients last year. However, much knowledge on PINK1 has been obtained from in vitro studies and very little is known on how the PINK1 pathway is regulated and functions in the brain and projects will be aimed at uncovering entirely new understanding of PINK1 function that may lead to new concepts for therapeutic exploitation in PD.The successful candidate(s) will benefit from an interdisciplinary environment in the Muqit Lab in the MRC PPU in Dundee. The laboratory forms part of the national UK DRI and the EMBO YIP networks and successful applicants will have access to UK DRI and EMBO sponsored opportunities for training and self-development. The MRC unit also collaborates a major pharmaceutical company that support the Division of Signal Transduction Therapy that provides opportunities for interaction with industry and potential exploitation of new discoveries made in the lab. The Lab actively participates in Public Engagement and successful candidates will be encouraged to be involved in public and patient involvement.
Overall, this position provides an exciting opportunity to be involved in world-class research projects and for the successful applicant to carve themselves a major international reputation. The successful candidate(s) will have an opportunity to be trained in a suite of state-of-the-art techniques during the project.
Your priorities will include:
- Primary mouse differentiation protocols to CNS cell types including neurons and astrocytes.
- Design and performing kinome-wide CRSIPR/Cas9 knock-down screen and sgRNA enrichment analysis.
- Proteomic discovery platforms including PTM proteomics and organellar isolation workflows
- Public and patient involvement and engagement presentations.
- Dissemination of protocols and data openly and through formal peer-reviewed publications.
- Advising and mentoring undergraduate and PhD students.
Candidate requirements:
- Have a PhD in Cell Biology, Mouse Neuroscience, Biochemistry, Proteomics or related discipline with outstanding academic track record and a publication record in internationally recognised peer-reviewed journals.
- Have a strong interest in signal transduction research and how disruptions of these pathways are linked to human disease.
- Have a strong background in mouse neurobiology, biochemistry, cell biology proteomics and/or gene editing.
- Have a strong ability to work independently but with excellent ability to work in a team, and an open and collaborative approach to science.
- Highly organised, motivated and meticulous, with an ability to work independently and to drive a project forward robustly and at pace.
- Have excellent communication skills and knowledge of the English language are essential.
- Prior experience in mouse neurobiology or proteomics would be highly desirable.
For further information about this position please contact Prof Miratul Muqit at m.muqit@dundee.ac.uk. To find out more about MRC PPU please visit https://www.ppu.mrc.ac.uk/
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Key details
- Location UK DRI at Cardiff
- Salary: This 3.5‑year studentship, funded by the Motor Neurone Disease Association, is available to 'Home' fee status. The award covers tuition fees and provides a maintenance stipend, which is ££21,383, for the 2026/7 academic year
About the Project
This studentship aims to investigate how mutations associated with rare familial forms of motor neurone disease (MND), disrupt lysosomal function in human motor neurons. Using a combination of patient-derived fibroblasts and iPSC-derived motor neurons carrying MND-associated mutations the studentship will characterise the impact of the mutations on lysosomal morphology, acidification, and Ca2+ handling. Quantitative assays, including ratiometric fluorescent imaging and automated confocal analysis, will be used to assess lysosomal morphology, distribution and function. In parallel, we will evaluate downstream consequences such as altered proteolytic activity and lipid accumulation. The student will explore therapeutic rescue of lysosomal defects using small molecule modulators of lysosomal function. Through detailed mechanistic and phenotypic analyses, this studentship seeks to establish how lysosomal dysregulation contributes to MND and to identify potential therapeutic targets relevant to a broader spectrum of MND patients.
Lead Supervisor- Dr Owen Peter
Entry Requirements:
As only one studentship is available and a very high standard of applications is typically received, the successful applicant is likely to have a very good first degree (a First or Upper Second class BSc Honours or equivalent) and/or be distinguished by having relevant research experience.
How to apply:
You can apply online - consideration is automatic on applying for a PhD with an October 2026 start date.
Entry Requirements:
As only one studentship is available and a very high standard of applications is typically received, the successful applicant is likely to have a very good first degree (a First or Upper Second class BSc Honours or equivalent) and/or be distinguished by having relevant research experience.
This 3.5‑year studentship, funded by the Motor Neurone Disease Association, is available to 'Home' fee status applicants and will begin on 1st October 2026. The award covers tuition fees and provides a maintenance stipend, which is ££21,383, for the 2026/27 academic year.
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Key details
- Location UK DRI at Cardiff
- Salary: This Wales Heart Research Institute Cardiovascular Fund studentship is open to Home and EU applicants. The award offered will cover fees and a maintenance stipend (for 26/27 this will be approx. £21,300).
About the Project
Background
Vascular dementia is the second most common type of dementia after Alzheimer’s disease and is caused by impaired blood supply to the brain. A key causative factor in the pathogenesis of vascular dementia is the development of atherosclerosis affecting the small blood vessels within the brain. Other cardiovascular events such as strokes (large and small) are also major contributory events in the development of the disease. Common “lifestyle” risk factors affecting the development of vascular dementia are identical to those identified for cardiovascular disease and include: high blood pressure, high cholesterol, diabetes, obesity, physical inactivity and smoking.
We have previously shown that the complement system, a key component of innate immunity comprising more than 40 different proteins is intimately involved in the development and progression of atherosclerosis. Thus, in developing atherosclerotic plaques complement is activated, causing an inflammatory response that drives the disease. The absence of key complement proteins of the “terminal” pathway ameliorates disease (Lewis et al 2010). More recently we have focused on the mechanisms underlying the genetically proven links between complement and Alzheimer’s Disease (AD). Here again, we have demonstrated that therapeutic blockade of complement activation in a mouse model of AD through the administration of blocking antibodies can slow the development of the disease and improve cognitive performance (Zelek W.M. et al 2024).
Modelling Dementia in animals relies largely on genetically altered mice carrying the human transgenes responsible for familial AD. This is not ideal since familial AD comprises only a small percentage of dementia cases. Recent publications have described, more relevant models to address the pathology of vascular dementia (Sweetat S. et al 2024, Kruyer A. et al 2015). Given the vascular damage and inflammation that has been documented in these new models we hypothesise that complement will be activated and play a significant contributory role in driving disease.
Aims
To test our hypothesis, we shall use the published ovariectomised model of vascular dementia where female mice are fed a diet high in fat, sugar and salt to mimic post-menopausal ageing together with several of the key risk factors relevant to human vascular dementia. The model will be used in three sets of experimental analyses:
1) We shall assess the extent of complement activation in these model mice. This will be carried out through the use of in-house ELISA-based assays and immunohistochemistry in the serum and brain tissues of these animals respectively.
2) We shall utilise in-house complement deficient strains (eg C7-/-; C3-/- and CD59) to understand the effect of deleting key complement genes in this model of vascular dementia.
3) We shall administer our previously validated anti-complement antibodies (anti C7) to determine whether complement blockade is a viable therapeutic approach to vascular dementia in this model.
Methodologies Employed
A range of techniques will be employed throughout this project to assess disease and test the effectiveness of our therapeutic approach. Thus, ELISA based assays, behavioural tests and immunohistochemistry staining for a range of markers in the brain tissues of these mice including (C3b; MAC; amyloid; tau; Iba-1; GFAP) will be utilised in all three aims. These will validate the model in our hands and allow assessment of the activation of complement. Furthermore, In the serum of model animals, Cytokines, Cholesterol, triglycerides, glucose and liver enzyme function will be assessed at baseline, during and at the end of each experiment. Where needed we shall confirm these findings by ELISA based analyses of total brain homogenates. RNA will be isolated and used in qPCR assessment of specific gene sets relevant to vascular dementia, neuroinflammation and complement. Supporting methodologies will include cell culture, protein purification and complement haemolysis assays to produce, purify and test the therapeutic antibodies that we will employ.
Potential Impact
This project will establish the extent of complement activation and its role in driving the progression of vascular dementia in a newly emerging relevant model of the vascular dementia. Data obtained will allow an assessment of the efficacy of inhibiting complement during the disease as a therapeutic approach. These outcomes could have important implications for how the second most common form of dementia is measured, and open new directions for therapeutic development.
How to apply:
Please use our online application service at: https://www.cardiff.ac.uk/study/postgraduate/research/programmes/programme/pharmacy
and specify in the funding section that you wish to be considered for WHRI funding.
Please also specify the project title and supervisor
The closing date for applications is 6th March 2026 and we expect interviews to be held in April
The successful applicant is likely to have a very good first degree (a First or Upper Second class Honours or equivalent)
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Key details
- Location UK DRI at Cardiff
- Salary: This Wales Heart Research Institute Cardiovascular Fund studentship is open to Home and EU applicants. The award offered will cover fees and a maintenance stipend (for 26/27 this will be approx. £21,300).
About the Project
Project summary:
Shock is a severe, life-threatening condition caused by critically reduced blood flow to tissues and organs and remains a major cause of death and disability in intensive care. A central feature of shock is endothelial dysfunction, leading to vascular leakage, tissue oedema, and multi-organ failure. Emerging evidence indicates that dysregulation of the complement system, a key component of innate immunity, contributes to this process by driving inflammation, amplifying coagulation, and promoting vascular injury. However, the precise complement pathways involved in cardiogenic shock (CS) and the prognostic value of circulating complement biomarkers remain unclear. This project will address these gaps by profiling complement dysregulation in CS using a comprehensive biomarker panel. The work will define the complement pathways driving vascular injury, identify predictive biomarker signatures, and highlight novel therapeutic targets to improve outcomes in critically ill patients.
Research plan
The student will analyse complement dysregulation in shock with the following aims:
Aim 1: Quantify complement components, regulators, and activation markers using 25 in-house complement assays (ELISA and/or MSD) in plasma from a unique cohort of >350 patients with cardiovascular shock, collected at Barts Health NHS Trust (Barts), alongside matched healthy controls.
Aim 2: Integrate complement biomarker data with clinical outcomes and biochemical measures (e.g. troponin, lactate, syndecan-1, vascular cell adhesion molecule-1 (VCAM-1)) to identify signatures associated with endothelial dysfunction and disease severity.
Aim 3: Develop predictive biomarker models using statistical and pathway analyses to identify marker sets associated with mortality, prolonged intensive care unit (ICU) stay, persistent organ dysfunction, and where longitudinal data permit (vascular cognitive impairment and vascular dementia) relevant outcomes, forming the basis for future vascular dementia; focused biomarker and therapeutic studies.
Techniques and training
The student will receive technique-rich training in complement immunoassays (ELISA, MSD), biomarker discovery pipelines, and translational cardiovascular immunology. They will gain experience in advanced biostatistics and machine-learning approaches (e.g. PCA, clustering, random forest) using R and Python, alongside assay development to industry standards, including analytical validation, quality control, and exposure to regulatory frameworks (ISO13485, IVDR principles). The student will be embedded within the Division of Infection and Immunity and the Cardiff Dementia Research Institute (DRI), a highly collaborative environment with a strong ECR network. They will be registered in the School of Medicine and supported by cross-school supervision and collaboration with the School of Biosciences, providing access to complementary expertise, facilities, and training opportunities.
Supervision and environment
The project will be jointly supervised by experts in complement biology, cardiovascular science, and data science:
Impact and career development
This project offers excellent interdisciplinary training at the interface of academic science, clinical medicine, and industry. It is well positioned to generate high-quality pilot data suitable for future BHF or NIHR applications and to deliver impactful research outputs relevant to cardiovascular and immunology research. The student will develop a robust skillset spanning complement biology, vascular inflammation, quantitative biomarker science, and statistical modelling, providing a strong foundation for a career in academia, translational research, or the biotech/pharmaceutical sector.
How to apply:
You can apply online - consideration is automatic on applying for a PhD with an October 2026 start date.
Please use our online application service at: https://www.cardiff.ac.uk/study/postgraduate/research/programmes/programme/pharmacy