Grade 7 (£31,604 - £38,833)
Medical Research Council Protein Phosphorylation and Ubiquitylation Unit
Professor Karim Labib will delve into the science behind the fabric of our very existence at the next Café Science event. Professor Labib from the MRCPPU will be talking about DNA and how it passes from one generation to the next. At the event, on Monday 13 November at Avery & Co, he will explain what this process can tell us about the evolution of life.
Protein malfunction, which can be caused by amplification or mutations, lies at the root of many human diseases. Therefore, individual proteins are often targeted for therapeutic interventions against many human diseases. However, it is thought that only a small percentage of proteins are ‘druggable’, meaning they can be targeted for therapeutic intervention by conventional drug approaches. The vast majority of the proteins still remain ‘undruggable’ and novel targeting strategies are required for us to be able to target these.
Postdoctoral position in the laboratory of Professor Dario Alessi FRS to unravel the role of signalling pathways linked to understanding regulation and function of the WNK signalling pathway.
Adrien Rousseau has opened a new laboratory in the MRC PPU to investigate signalling pathways controlling proteasome homeostasis.
A major goal of Adrien’s laboratory will be to unravel the crosstalk between protein phosphorylation and ubiquitin proteasomal degradation pathways. The aim is to better understand how cells prevent accumulation of unfolded, misfolded, or damaged proteins that is deleterious and an underlying cause of various age-related diseases, including cancers and neurodegenerative disorders.
John Rouse, together with researchers Detlev Schindler at the University of Wuerzburg, and Minoru Takata at the University of Kyoto, have won the Fanconi Anemia Research Fund 2017 Discovery Award for the discovery and characterization of the Fanconi anemia gene FANCW. Commenting on the award John said: “I’m delighted that our work on FANCW should be recognized by the Fanconi Anemia Research Fund.
Within the epithelial layers of our barrier surfaces resides a complex and unconventional pool of T cells collectively called intraepithelial lymphocytes (IEL). At the intestine, IEL patrol the single layer of epithelium that lies between the external environment exposed to chemicals, food, and pathogens, and the sterile internal environment. Due to their strategic placement, intestinal IEL are the first immune cells that come in contact with potentially harmful agents, and are tasked with eliminating infected or damaged epithelial cells, and maintaining mucosal homoeostasis.
Intraepithelial lymphocytes (IEL) are the first immune cells that pathogens encounter in the gut. These T lymphocytes lie within the epithelial layer, and are central to controlling infection, stress or transformation of the gut epithelium. At the same time, deregulation of IEL responses can lead to inflammatory bowel diseases such as colitis and Crohn’s disease. Despite their importance, we have a poor understanding of how IEL sense and respond to stress and infection of the intestinal epithelia, and how they maintain their quiescence in the presence of the normal gut microflora.
Intellectual disability is a genetically heterogeneous and poorly understood developmental disorder estimated to affect 1-2% of the world’s population. The X-chromosome is a critical centre for genes involved in intellectual development, and X-Linked Intellectual Disability (XLID) forms an important class of intellectual disability. Despite the large number of genetic studies in this area, the molecular mechanisms underpinning intellectual disability remain unknown. Recently, mutations in the X-linked RNF12/RLIM E3 ubiquitin ligase were identified as drivers of XLID.