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ELAV/Hu proteins inhibit p27 translation via an IRES element in the p27 5 ' UTR

MPS-Authors
http://pubman.mpdl.mpg.de/cone/persons/resource/persons78286

Kullmann,  M.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78017

Göpfert,  U.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78709

Siewe,  B.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78092

Hengst,  L.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

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Citation

Kullmann, M., Göpfert, U., Siewe, B., & Hengst, L. (2002). ELAV/Hu proteins inhibit p27 translation via an IRES element in the p27 5 ' UTR. Genes & Development, 16(23), 3087-3099.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0010-6DBE-E
Abstract
p27(Kip1) restrains cell proliferation by binding to and inhibiting cyclin-dependent kinases. To investigate the mechanisms of p27 translational regulation, we isolated a complete p27 cDNA and identified an internal ribosomal entry site (IRES) located in its 5'UTR. The IRES allows for efficient p27 translation under conditions where cap-dependent translation is reduced. Searching for possible regulators of IRES activity we have identified the neuronal ELAV protein HuD as a specific binding factor of the p27 5'UTR. Increased expression of HuD or the ubiquitously expressed HuR protein specifically inhibits p27 translation and p27 IRES activity. Consistent with an inhibitory role of Hu proteins in p27 translation, siRNA mediated knockdown of HuR induced endogenous p27 protein levels as well as IRES-mediated reporter translation and leads to cell cycle arrest in G1.