Standing out in the field of IgY Immunotechnology

  • Home
    Home A full collection of all the Research Archive entries.
  • Years
    Years Sort entries by year.
  • Tags
    Tags Displays a list of tags that have been used in the blog.
  • Archives
    Archives Contains a list of research entries that were created previously.

Fragile mental retardation protein interacts with the RNA-binding protein Caprin1 in neuronal RiboNucleoProtein complexes.

Posted by on in 2012
  • Font size: Larger Smaller
  • Hits: 1592
  • Print

El Fatimy R, Tremblay S, Dury AY, Solomon S, De Koninck P, Schrader JW, Khandjian EW. 2012. PLoS One. 7(6):e39338. Epub 2012 Jun 21.

Centre de Recherche, Institut Universitaire en Santé Mentale, Québec, PQ, Canada.


Abstract

Fragile X syndrome is caused by the absence of the Fragile X Mental Retardation Protein (FMRP), an RNA-binding protein. FMRP is associated with messenger RiboNucleoParticles (mRNPs) present in polyribosomes and its absence in neurons leads to alteration in synaptic plasticity as a result of translation regulation defects. The molecular mechanisms by which FMRP plays a role in translation regulation remain elusive. Using immunoprecipitation approaches with monoclonal Ab7G1-1 and a new generation of chicken antibodies, we identified Caprin1 as a novel FMRP-cellular partner. In vivo and in vitro evidence show that Caprin1 interacts with FMRP at the level of the translation machinery as well as in trafficking neuronal granules. As an RNA-binding protein, Caprin1 has in common with FMRP at least two RNA targets that have been identified as CaMKIIα and Map1b mRNAs. In view of the new concept that FMRP species bind to RNA regardless of known structural motifs, we propose that protein interactors might modulate FMRP functions.

PMID:
    22737234
    [PubMed - in process] 


PMCID:
    PMC3380850

Last modified on