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QUAKING KH Domain Proteins as Regulators of Glial Cell Fate and Myelination
Daniel Larocque and Stéphane Richard
volume 2 | issue 2
april/may/june 2005Pages: 37 - 40
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The quaking viable (qkv) mice have always attracted attention because of their characteristic tremor caused by their dysmyelination. In the central nervous system, qkv mice fail to develop mature myelinating oligodendrocytes and display uncompacted myelin. The genetic defect in the qkv mice prevents the proper expression of alternatively spliced KH-type QKI RNA binding proteins. Thus qkv mice provide a unique animal model linking RNA binding proteins to defects in oligodendrocyte cell fate and myelination. The fact that QKI proteins are modified post-translationally makes them Signal Transduction Activiators of RNA (STAR) proteins. We have used a gain-of-function approach with the ectopic expression of the separate QKI isoforms using adenoviruses and retroviruses to determine their separate roles in cell fate and myelination. Herein, we discuss the recent advances in characterizing the QKI KH-type proteins as glial cell fate and myelin regulators.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.