Mice lacking Snrpn expression show normal regulation of neuronal alternative splicing events

John D. Huntriss, Jacqueline A. Barr, David A. Horn, David G. Williams, David S. Latchman

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

The SmN protein is closely related to the constitutively expressed RNA splicing protein SmB but is expressed only in brain and heart tissue. Mice which lack expression of SmN die shortly after birth suggesting a critical role for this protein possibly in the regulation of neuronal-specific alternative splicing events. We show here however that the neuronal-specific alternative splicing of the RNAs encoding several different classes of protein proceeds normally in mice lacking SmN expression. The potential role of SmN and the reasons for the lethal effect observed in non-expressing mice are discussed.

Original languageEnglish
Pages (from-to)19-25
Number of pages7
JournalMolecular Biology Reports
Volume20
Issue number1
DOIs
Publication statusPublished - Jul 1994

Keywords

  • alternative splicing
  • imprinting
  • Prader-Willi syndrome
  • SmN

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