Alternative splicing: multiple control mechanisms and involvement in human disease.

By J. Cáceres, A. Kornblihtt. Trends in Genetics, 2002

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A slow RNA polymerase II affects alternative splicing in vivo. (2003, background): “To explain this, a kinetic coupling model has been proposed, where the transcript elongation rate determinesSummary the outcome of competing splicing reactions that occur cotranscriptionally (Cáceres and Kornblihtt, 2002).”
Pre-mRNA splicing and human disease. (2003, background): “Cis-acting mutations have been tabulated in several reviews and the Human Gene Mutation Database (HGMD, http://www.uwcm.ac.uk/uwcm/ mg/hgmd0.html; Nakai and Sakamoto 1994; Cooper et al. 1995; Rogan et al. 1998; Caceres and Kornblihtt 2002; Cartegni et al. 2002).”
Epigenetics in alternative pre-mRNA splicing (2011, positive): “The importance of alternative splicing is dramatically highlighted by the numerous diseases that are caused by mutations in either cis-acting RNA elements or trans-acting protein splicing factors (Caceres and Kornblihtt, 2002; Cooper et al., 2009).”
Opportunities and challenges Genome-wide analyses of alternative splicing in plants: (2008, positive): “Some hnRNP proteins have been demonstrated to silence splicing (Hastings and Krainer 2001; Caceres and Kornblihtt 2002; Szeszel-Fedorowicz et al. 2006).”