The inclusion or skipping of the exon depends on two antagonistic proteins, TIA-1 and polypyrimidine tract-binding protein (PTB).
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The Sxl protein is a splicing repressor that binds to an ISS in the RNA of the Tra transcript near the upstream acceptor site, preventing U2AF protein from binding to the polypyrimidine tract.
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However, two isoforms, the apoptosis-inducing membrane-bound form and the soluble form, are normal products whose production via alternative splicing is regulated by the cytotoxic protein TIA1.
After being produced, the stability and distribution of the different transcripts is regulated (post-transcriptional regulation) by means of RNA binding protein (RBP) that control the various steps and rates of the transcripts: events such as alternative splicing, nuclear degradation (exosome), processing, nuclear export (three alternative pathways), sequestration in DCP2-bodies for storage or degradation, and ultimately translation.
The drug is speculated to modulate the alternative splicing of the SMN2 gene, increasing the amount of the SMN protein whose deficiency is regarded as the root cause of the disease.
TNPO3 is a nuclear import receptor for serine/arginine-rich (SR) proteins, including Serine/arginine-rich splicing factor 1, which are essential precursor-mRNA splicing factors.
There is evidence that a truncated form of MBII-52 (SNORD115 found in mouse) regulates the alternative splicing of the protein coding genes DPM2, TAF1, RALGPS1, PBRM1, and CRHR1.