英国曼彻斯特大学分子与细胞生物学博士后职位

POSTDOCTORAL SCIENTIST – Dr Angeliki Malliri Cell Signalling Group

• Salary in the range of £28,500 – £38,000 dependent upon qualifications and experience
• Job Ref: MI/14/25
• 3 year position

The Cancer Research UK Manchester Institute (www.cruk.manchester.ac.uk), an Institute of The University of Manchester (www.manchester.ac.uk), is a world-leading centre for excellence in cancer research. The Institute is core funded by Cancer Research UK (www.cancerresearchuk.org), the largest independent cancer research organisation in the world. We are adjacent to The Christie NHS Foundation Trust (www.christie.nhs.uk), one of the largest cancer treatment centres in Europe. These factors combine to provide an exceptional environment in which to pursue basic, translational and clinical research programmes.
Our aim is to understand the fundamental basis of cancer and apply that knowledge to developing new treatment strategies for cancer patients. Our advanced research programmes span a spectrum of cancer research, from the molecular and cellular basis of cancer through to drug discovery, translational research and clinical trials.

The Institute has outstanding laboratory facilities and exceptional core services, including next generation sequencing, microarrays, confocal microscopy, bioinformatics, histology and mass-spectrometry.
We are situated in Manchester, England, a vibrant and dynamic city that is surrounded by beautiful countryside and has excellent transport links both nationally and internationally.
A 3 year position is available in the laboratory of Dr Angeliki Malliri. Her group is investigating the role of RAC signalling in neoplastic transformation. The successful applicant will study the role of Tiam2/STEF alone or in combination with Tiam1 in the development of cancer using in vivo models recently generated as well as organoid culture models.

The successful applicant should have a PhD in molecular and cellular biology. A background working with in vivo models is highly desirable but not essential.

Recent relevant publications from our lab include:
Mack et al. (2012) β2-syntrophin and Par-3 promote an apicobasal Rac activity gradient at cell-cell junctions by differentially regulating Tiam1 activity. Nature Cell Biology 14, 1169.
Castillo-Lluva et al. (2010) SUMOylation of the GTPase Rac1 is required for optimal cell migration. Nature Cell Biology 12, 1078.
Woodcock et al. (2009) Src-induced disassembly of adherens junctions requires localized phosphorylation and degradation of the Rac activator Tiam1. Molecular Cell 33, 639.
Rooney et al. (2010) The Rac activator STEF (Tiam2) regulates cell migration by microtubule-mediated focal adhesion disassembly. EMBO Rep. 11, 292.