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Molecular regulation of surface remodelling in the human pathogen Schistosoma mansoni

  • Full or part time
  • Application Deadline
    Applications accepted all year round
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

Project Description

In this PhD project you will perform cutting edge research that aims to identify molecular signalling events that underpin the survival of schistosomes in their human host.

Schistosomes are parasites that cause human schistosomiasis, a neglected tropical disease affecting over 260 million people across the globe. The parasite can survive in its human host for many years and key to this survival is the tegument, a surface layer that envelopes the parasite and interacts with host blood. Aside from being a protective layer against immune attack, molecular communication from the host across this layer is considered important to the growth, development and survival of the parasite.

This project aims to characterise important molecular signalling events that underpin the initial development and maintenance of the schistosome tegumental surface layer and its components, particularly in parasites that are transforming into human host-resident life stages. The project will investigate the importance of a range of proteins (such as protein kinases) to these processes, particularly in relation to molecular signalling from the host. A better understanding of the processes that drive tegument evolution and integrity may lead to the development of novel drugs to kill schistosomes and thus stem schistosomiasis disease transmission.

This project offers an excellent opportunity to become trained in molecular parasitology. Working alongside other molecular parasitolgists you will become highly skilled in techniques such as immunohistochemistry and confocal laser scanning microscopy, protein analysis and RNA interference.

Candidates must demonstrate strong interest in molecular and/or medical parasitology, have appropriate training/educational background in relevant areas and satisfy Kingston University entry requirements. In all cases a master’s degree or equivalent qualification or other evidence of research skills and experience is preferred but not essential.

Funding Notes

No funding is available for this project: applications can only be accepted from self-funded candidates

References

Ressurreição M, Elbeyioglu F, Kirk RS, Rollinson D, Emery AM, Page NM, Walker AJ (2016). Molecular characterization of host-parasite cell signalling in Schistosoma mansoni during early development. Scientific Reports 6:35614 (16 pg).

Hirst NL, Lawton SP, Walker AJ (2016). Protein kinase A signalling in Schistosoma mansoni cercariae and schistosomules. International Journal for Parasitology 46: 425-437.

Ressurreição M, Kirk RS, Rollinson D, Emery AM, Page NM, Walker AJ (2015). Sensory protein kinase signalling in Schistosoma mansoni cercariae: host location and invasion. The Journal of Infectious Diseases 212: 1787-1797.

Walker AJ, Ressurreição M, Rothermel R (2014). Exploring the function of protein kinases in schistosomes: perspectives from the laboratory and from comparative genomics. Frontiers in Genetics, 5: 229 (9 pg).

Ressurreição M, De Saram PSR, Kirk RS, Rollinson D, Emery AM, Page NM, Davies AJ, Walker AJ (2014). Protein kinase C and extracellular signal-regulated kinase regulate movement, attachment, pairing and egg release in the human blood fluke Schistosoma mansoni. PLoS Neglected Tropical Diseases 8: e2924 (21 pg)

De Saram PSR, Ressurreição M, Davies AJ, Rollinson D, Emery AM, Walker AJ (2013). Functional mapping of protein kinase A reveals its importance in adult Schistosoma mansoni motor activity. PLoS Neglected Tropical Diseases 7, e1988 (15 pg)

2011 Walker AJ (2011). Insights into the functional biology of schistosomes. Parasites & Vectors 4, 203 (6 pg)

How good is research at Kingston University in Allied Health Professions, Dentistry, Nursing and Pharmacy?

FTE Category A staff submitted: 17.22

Research output data provided by the Research Excellence Framework (REF)

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