Sentence examples for binding of the splicing from inspiring English sources

Studying another silent mutation (c.807C > T), we predicted the abnormal splicing of exon 6 due to the disrupted binding of the splicing regulatory proteins.

Intriguingly it was recently shown that in HD a short transcript of the HTT gene is produced by aberrant splicing, probably influenced by abnormal binding of the splicing factor SRSF6 to the CAG repeat expansion [ 19].

In addition, we found one member of the hnRNPs family to be repressed, which is of interest since members of the hnRNPs competitively inhibits binding of the splicing factors to the immature mRNA [ 44].

We show that the mutation exerts its pathogenicity by creating a general ESE motif, which is also important in another gene and functions by binding of the splicing regulatory protein SF2/ASF (splicing factor 2/alternative splicing factor).

Altogether, these data suggested that the c.903+469T>C mutation activates the pseudoexon by strengthening and/or creating an ESE, which potentially could function by binding of the splicing factor SF2/ASF.

The cause of the deletion is not easy to ascertain, but could be attributable to changes in the RNA secondary structure induced by this SNP, which could alter binding of the splicing machinery.

U2 snRNP binding to the 3' splice site of exon 7 is impaired in SMN2 compared with SMN1 (22, 59).

This indicates that although suppression of pseudoexon splicing by U1snRNP binding outside of the splice site can suppress some pseudoexons, it is not a general feature of all pseudoexons.

The proximity of cis-regulatory sequences, either enhancers or silencers of exon or intron splicing, influences the binding of different trans-splicing factors to the splice sites and aids assembly of the spliceosome multi-protein complex, resulting in cleavage and ligation of introns and exons, respectively [ 32, 33].

In MALAT1-depleted cells, the expression of an oncogenic transcription factor, B-MYB (Mybl2), which is involved in G2/M progression, is reduced because of the aberrant binding of splicing factors and abnormal alternative splicing [ 23].

The successive binding of PTB may itself be regulatory by interfering with the binding of other splicing factors, and/or functioning to create a scaffold on the pre-mRNA through the molecular interactions between the bound PTB proteins.