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The role of the p53 co-factor JMY in the regulation of gene expression in human cancer

  • Full or part time
    Dr A Coutts
  • Application Deadline
    Thursday, April 04, 2019
  • Funded PhD Project (Students Worldwide)
    Funded PhD Project (Students Worldwide)

Project Description

Tumour growth is achieved by overriding cell cycle control and bypassing cell death mechanisms. Mechanisms influencing cell survival such as apoptosis and autophagy are key determinants of cell fate during stress. Moreover, during tumour progression the acquisition of metastatic potential is the most devastating event in human cancer with metastatic disease the cause of 90% of cancer deaths. Importantly, understanding how the cell integrates a variety of signals to affect a cellular outcome is clinically relevant and a poorly understood process.

p53 is a nuclear transcription factor that plays a pivotal role in the prevention of human cancer in part through its role during cellular stress which results in a variety of outcomes such as cell cycle arrest, autophagy or apoptosis. The critical importance of p53 function is highlighted by the fact that the majority of human tumours harbour compromised p53 activity. JMY is a p53 transcriptional co-factor that accumulates in the nucleus during the DNA damage response to influence p53-dependent apoptosis. This project will investigate the nuclear targets of JMY in order to identify genes whose activity influences cell fate during the stress response and the mechanisms involved. This work will involve a range of cell and molecular biology techniques including RNA-Seq, bio-informatics, microscopy, cell-based assays and chemical biology techniques.

An appropriate student will have a good background in biochemistry and cell biology together with an enthusiasm and strong desire to understand molecular mechanism related to cancer biology.

Applicants should hold, or be expected to hold, a Master’s degree with a minimum of a commendation, and/or a 1stClass / 2.1 Bachelor’s Honour’s Degree (or UK equivalent) in Cell Biology, Biochemistry, Molecular Biology, or a related Biosciences related subject.

Funding Notes

This is a fully funded NTU studentship, covering UK/EU fees and paying a stipend in line with UKRI.

Applications from non-EU students are welcome, but a successful candidate would be responsible for paying the difference between non-EU and UK/EU fees.

References

Coutts AS, La Thangue NB. Actin nucleation by WH2 domains at the autophagosome. Nat Commun, 6: 2015. DOI: 10.1038/ncomms8888.

Coutts AS, Pires IM, Weston L, Buffa FM, Milani, M, Li J-L, Harris AL, Hammond EM and La Thangue NB. Hypoxia-driven cell motility reflects the interplay between JMY and HIF-1a Oncogene, 30: 4835-4842, 2011.

Coutts AS, Weston L, and La Thangue NB. A transcription co-factor integrates cell adhesion and motility with the p53 response. PNAS., 106: 19872-19877, 2009.

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

FTE Category A staff submitted: 23.80

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

Click here to see the results for all UK universities

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