Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Pre-mRNA Splicing

  • Dawn S. Chandler
Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_4711-2

Definition

Splicing is a tightly regulated mechanism for the control of gene expression that involves the precise removal of introns from the precursor mRNA molecule and the subsequent ligation of the remaining exons.

Characteristics

Premature RNAs that are transcribed within the cell nucleus contain both coding sequences (contained within functional units called exons) and noncoding sequences that are eventually excised. Splicing is the mechanism by which the noncoding portions of the RNA (also known as introns) are removed from pre-mRNAs, via two cleavage-ligation reactions, each involving transesterification at a splice site phosphate (see Fig. 1). Ultimately, the two exons are ligated to generate the spliced mRNA, and the excised intron is released in a lariat configuration that is eventually degraded. The splicing reaction has been well defined and is mediated by the dynamic ordered assembly of numerous spliceosome components directly on the pre-mRNA. To avoid the production of...

Keywords

Splice Site Sodium Butyrate Intron Retention Splice Regulation Splice Machinery 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

  1. Black DL (2003) Mechanisms of alternative pre-messenger RNA splicing. Annu Rev Biochem 72:291–336CrossRefPubMedGoogle Scholar
  2. Cartegni L, Chew SL, Krainer AR (2002) Listening to silence and understanding nonsense: exonic mutations that affect splicing. Nat Rev Genet 34:285–298CrossRefGoogle Scholar
  3. Chandler D (2007) Splicing of the p53 pathway. In: Venables J (ed) Alternative splicing in cancer. Transworld Research Network, NewcastleGoogle Scholar
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  5. Venables JP (2004) Aberrant and alternative splicing in cancer. Cancer Res 64(21):7647–7654CrossRefPubMedGoogle Scholar

See Also

  1. (2012) Exon. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1360. doi:10.1007/978-3-642-16483-5_2059Google Scholar
  2. (2012) Exonic splicing enhancer. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1361. doi:10.1007/978-3-642-16483-5_2060Google Scholar
  3. (2012) Intron. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1904. doi:10.1007/978-3-642-16483-5_3131Google Scholar
  4. (2012) Pre-mRNA. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 2972. doi:10.1007/978-3-642-16483-5_4710Google Scholar
  5. (2012) SnRNP. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3460. doi:10.1007/978-3-642-16483-5_5398Google Scholar
  6. (2012) Spliceosome. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3487. doi:10.1007/978-3-642-16483-5_5455Google Scholar
  7. (2012) SR proteins. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3495. doi:10.1007/978-3-642-16483-5_5463Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Department of Pediatrics, Columbus Children’s Research Institute, Center for Childhood CancerThe Ohio State University School of MedicineColumbusUSA