Postdoc positions at the CRUK London Research Institute

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Postdoc positions at the CRUK London Research Institute

Postby mcramel » Tue May 25, 2010 10:28 am

Two postdoctoral positions are available in the laboratory of Dr Caroline Hill at the Cancer
Research UK London Research Institute, Lincoln’s Inn Fields, London. One is available
immediately and another later in the year.

The lab is focused on studying TGF-β superfamily signalling pathways. We want to understand
how these signalling pathways function normally in early vertebrate development and in adult
untransformed tissue culture cells, and how they are perturbed in cancer. We use a wide variety
of model systems (Xenopus, zebrafish and mice, as well as tissue culture and in vitro systems) and
methodologies ranging from developmental and cell biology to computational modelling.

I am looking for highly motivated postdocs with proven research abilities and an excellent
publication record. Prior experience in molecular biology is essential and experience in animal
models is highly desirable. Postdoctoral Fellowships are available for a period of 4 years. Annual
salary in the range of £25,500 - £33,000 plus a London Living Allowance of £3750. The
laboratory is based at 44 Lincoln’s Inn Fields in Central London.

For further details about the projects please contact
Dr Caroline Hill

Selected References:
Wu MY and Hill CS. (2009) Dev Cell. 16, 329-343. TGF-β superfamily signaling in embryonic development
and homeostasis.
Daly AC, Randall RA, and Hill CS. (2008) Mol Cell Biol. 28, 6889-6902 Transforming growth factor
-β induced Smad1/5 phosphorylation in epithelial cells is mediated by novel receptor complexes and is
essential for anchorage-independent growth
Schmierer, B., Tournier, A.L., Bates, P.A. and Hill, C.S. (2008) Proc. Natl. Acad. Sci. USA 105, 6608-6613.
Mathematical modelling identifies Smad nucleocytoplasmic shuttling as a dynamic signalinterpreting
Schmierer, B. and Hill, C.S. (2007) Nature Rev. Mol. Cell Biol. 8, 970-982. TGF-β/Smad
signal transduction: molecular specificity and functional flexibility.
Levy, L., Howell, M., Das, D., Harkin, S., Episkopou, V., and Hill, C.S. (2007) Mol. Cell. Biol.
27, 6068-6083. Arkadia activates Smad3/Smad4-dependent transcription by triggering
signal-induced SnoN degradation.
Batut, J., Howell, M., Hill, C.S. (2007) Dev Cell. 12, 261-274. Kinesin-mediated transport
of Smad2 is required for signaling in response to TGF- ligands.
Ross, S., Cheung, E., Howell, M., Petrakis, TG., Kraus, W.L. and Hill, C.S. (2006) EMBO J. 25,
4490-4502. Smads orchestrate specific histone modifications and chromatin remodeling to
activate transcription.
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