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Protein Found to Be Essential For Maintaining Nerve Health

A team of researchers led by Michael Kiebler at the Max Planck Institute for Developmental Biology in Tübingen (now at the Center for Brain Research, University of Vienna), have been able to identify a // protein that seems to play a vital role in maintaining the overall health of the nerve cell.

The protein called Staufen2, appears to play a key role in the maintenance of synapses. The researchers found that if this protein was blocked out from a nerve cell, it lost a number of synapses. Synapses are the impulses that connect one nerve cell to the other and thus transmit information through various nerve cells. In the current study, appearing in the January 17 issue of the Journal of Cell Biology, researchers tried to analyze the effect of the loss of Staufen proteins from a nerve cell. These proteins are thought to be involved in transport of molecular blueprints (mRNAs) to specific locations in the cell. Nerve cells transmit information through highly specialized contact sites called as synapses. Proteins are very necessary for the maintenance of these synapses. But protein synthesis at a synapse is possible only when the mRNAs carrying the 'blueprint' arrive at the location. Staufen2 protein has been found to play a key role in this transportation process. Researchers Bernhard Goetze and Paolo Macchi have proved for the first time that Staufen2 is important for the maintenance of synapses. We wanted to know if Staufen2-deficient nerve cells can still transmit signals, said Michael Kiebler. Researchers also teamed up with Stefan Boehms group at the Medical University of Viennas Institute of Pharmacology. This particular research throws light on the intricate mechanisms involved in the brain's ability to learn and to memorize information.

Original work: Goetze B, Tuebing F, Xie Y, Dorostkar MM, Thomas S, Pehl U, Boehm S, Macchi P, and Kiebler MA The brain-specific double-stranded RNA binding protein Staufen2 is required for dendritic spi ne morphogenesis. Journal of Cell Biology, Vol. 172 (2), 17 January 2006

Contact Dr. Michael Kiebler Max-Planck-Gesellschaft

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