A method of identifying latent splice sites, the method comprising identifying at least one intronic in-frame stop codon located upstream of a 5' splice site sequence being a latent splice site, thereby identifying latent splice sites.

The 3' splice site or splice acceptor site terminates the intron with an almost invariant AG sequence.

The cell line has a unique splice site mutation of the NF2 gene.

Exon 11 contains an alternative splice site which removes 66 nucleotides from the open reading frame.

The 5' -donor splicing site sequence can be present in multiple copies, for example as a tandem repeat.

The target sequence is mature ribosomal RNA or at the splice site between a pre-ribosomal RNA tail and mature ribosomal RNA.

Included are methods of topically applying to the subject an effective amount of an antisense composition targeting the start site or splice site of a CFLAR mRNA.

Fifteen mutations were nonsense, frameshift or splice site alterations predicted to result in truncated proteins lacking phosphatase activity.

In one embodiment the 5 -donor splicing site sequence has the sequence 5' -MAGGTRAGTA-3' where M is A or C and R is A or G.

Phosphorylation of the alternative mRNA splicing factor 45 (SPF45) by Clk1 regulates its splice site utilization, cell migration and invasion.

Quantification of the hazards associated with introns reveals that mutations at key splice-site residues are a major source of human mortality.

hazards associated with introns reveals that mutations at key splicesite residues are a major source of human mortality.

This may, therefore, result in a deletion of an entire exon of the peptide sequence, the exon is not recognized because the splice site has been mutated.

There is provided a method of inhibiting gene expression by locating a 5' -5 donor splicing site sequence in the 3' UTR of a gene or within coding sequence containing the stop codon of a gene.