A Ph.D student position is available to study the regulation of alternative splicing by cellular signals in the group headed by Stefan Stamm at the University of Erlangen, Germany
The project aims to understand how cAMP dependent signals promote alternative exon inclusion in the SMN2 (survival of motor neuron 2) gene, which could be the basis to treat spinal muscular atrophy. We address this questions using a large variety of methods that range from state of the art molecular biology techniques to bioinformatics.
We are looking for a motivated, hard-working, bright and goal-oriented colleague that likes to work in a multicultural environment.
We offer excellent research facilities, a stimulating atmosphere and interesting, challenging projects that are published in leading journals. Citizens of the EU associated states in Eastern Europe and Israel are encouraged to apply, since a large amount of our funding comes from the European Union. It is possible that the laboratory will move to the United States in 2008.
More information can be found at: www. Stamms-lab.net
Please indicate why you are interested in this position and by 17th September 2006 send your CV as well as the names and e-mails of three persons willing to write a letter of recommendation to
dominique@stamms-lab.net
Selected references from the laboratory:
Kishore, S., and Stamm, S. (2006). The snoRNA HBII-52 regulates alternative splicing of the serotonin receptor 2C. Science 311, 230-232.
Rafalska, I., Zhang, Z., Benderska, N., Wolff, H., Hartmann, A. M., Brack-Werner, R., and Stamm, S. (2004). The intranuclear localization and function of YT521-B is regulated by tyrosine phosphorylation. Hum Mol Genet 13, 1535-1549.
Stoilov, P., Daoud, R., Nayler, O., and Stamm, S. (2004). Human tra2-beta1 autoregulates its protein concentration by influencing alternative splicing of its pre-mRNA. Hum Mol Genet 13, 509-524.
Daoud, R., Mies, G., Smialowska, A., Oláh, L., Hossmann, K., and Stamm, S. (2002). Ischemia induces a translocation of the splicing factor tra2-beta1 and changes alternative splicing patterns in the brain. J Neurosci 22, 5889-5899.