The connection between splicing and cancer
Top Cited Papers
Open Access
- 1 July 2006
- journal article
- review article
- Published by The Company of Biologists in Journal of Cell Science
- Vol. 119 (13) , 2635-2641
- https://doi.org/10.1242/jcs.03053
Abstract
Alternative splicing is a crucial mechanism for generating protein diversity. Different splice variants of a given protein can display different and even antagonistic biological functions. Therefore, appropriate control of their synthesis is required to assure the complex orchestration of cellular processes within multicellular organisms. Mutations in cis-acting splicing elements or changes in the activity of constitutive or alternative splicing could have a profound regulatory proteins that compromise the accuracy of either impact on human pathogenesis, in particular in tumor development and progression. Mutations in splicing elements, for example, have been found in genes such as LKB1, KIT, CDH17, KLF6 and BRCA1, and changes in trans-acting regulators can affect the expression of genes such as Ron, RAC1 and CD44.Keywords
This publication has 71 references indexed in Scilit:
- Complex networks orchestrate epithelial–mesenchymal transitionsNature Reviews Molecular Cell Biology, 2006
- Concerted regulation of nuclear and cytoplasmic activities of SR proteins by AKTNature Structural & Molecular Biology, 2005
- Inactivation of the SR Protein Splicing Factor ASF/SF2 Results in Genomic InstabilityCell, 2005
- SRprises along a Messenger’s JourneyMolecular Cell, 2005
- Cell signalling and the control of pre-mRNA splicingNature Reviews Molecular Cell Biology, 2004
- An extensive network of coupling among gene expression machinesNature, 2002
- Listening to silence and understanding nonsense: exonic mutations that affect splicingNature Reviews Genetics, 2002
- New functions for the matrix metalloproteinases in cancer progressionNature Reviews Cancer, 2002
- Initial sequencing and analysis of the human genomeNature, 2001
- A Novel Spliceosome Containing U11, U12, and U5 snRNPs Excises a Minor Class (AT–AC) Intron In VitroCell, 1996