Loss of the imprinted snoRNA mbii-52 leads to increased 5htr2c pre-RNA editing and altered 5HT2CR-mediated behaviour.

@article{Doe2009LossOT,
  title={Loss of the imprinted snoRNA mbii-52 leads to increased 5htr2c pre-RNA editing and altered 5HT2CR-mediated behaviour.},
  author={Christine M. Doe and Dinko Relkovic and Alastair S. Garfield and Jeffrey W. Dalley and David E. H. Theobald and Trevor Humby and Lawrence Stephen Wilkinson and Anthony R Isles},
  journal={Human molecular genetics},
  year={2009},
  volume={18 12},
  pages={
          2140-8
        }
}
The Prader-Willi syndrome (PWS) genetic interval contains several brain-expressed small nucleolar (sno)RNA species that are subject to genomic imprinting. In vitro studies have shown that one of these snoRNA molecules, h/mbii-52, negatively regulates editing and alternative splicing of the serotonin 2C receptor (5htr2c) pre-RNA. However, the functional consequences of loss of h/mbii-52 and subsequent increased post-transcriptional modification of 5htr2c are unknown. 5HT2CRs are important in… CONTINUE READING

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