Lena Wedeken

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Name: Lena Wedeken
Diploma / M.Sc degree: Philipps-University of Marburg, Germany
(November 2006)

PhD Project: The role of the RNA-binding activity of the tumor suppressor Pdcd4 in translational regulation

Abstract of Research Project

Gene expression is not only tightly controlled at the level of transcription but also on the level of translation. Enhanced protein synthesis contributes to the to the pathogenesis of diseases, such as cancer. Control of translation occurs primarily at the initiation step and can affect either global protein synthesis or only the translation of specific mRNAs. Both types of control represent key mechanisms of gene modulation.

The Pdcd4 (Programmed cell death 4) gene is a novel but as yet only poorly characterised tumor suppressor gene that has been implicated in the development of several kinds of cancer. The Pdcd4 protein is a nuclear-cytoplasmic shuttling protein that has been shown to interact with eukaryotic translation initiation factors eIF4A and eIF4G and to suppress the translation of 5' structured mRNAs. It was also shown to have intrinsic RNA-binding activity but the role of this activity for its molecular function still needs to be unraveled.

My research project is the further analysis of Pdcd4-RNA interactions with regard to two questions: a) Is Pdcd4 involved in general translation control or does it serve rather as a selective translational inhibitor? b) Does the RNA-binding activity of Pdcd4 play a role for its function in the cell?



Publications

L. Wedeken, P. Singh, K.-H. Klempnauer
Tumor suppressor protein Pdcd4 inhibits translation of p53 mRNA
J. Biol. Chem. 286(50) (2011), 42855-62.

P. Singh, L. Wedeken, L. C. Waters, M. D. Carr, K.-H. Klempnauer
Pdcd4 directly binds the coding region of c-myb mRNA and suppresses its translation
Oncogene. 30(49) (2011), 4864-73.

L. Wedeken, J. Ohnheiser, B. Hirschi, N. Wethkamp, K.-H. Klempnauer
Association of Tumor Suppressor Protein Pdcd4 With Ribosomes Is Mediated by Protein-Protein and Protein-RNA Interactions
Genes Cancer. 1(3) (2010), 293-301.


Lena Wedeken
eMail: Lena Wedeken