Skip to main content
Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Targeting RNA splicing modulation: new perspectives for anticancer strategy?

Fig. 1

The regulation mechanism and mode of RNA splicing. (A) Pre-mRNA includes 5’ splice sites (5’ ss), 3’ splice sites (3’ ss), branch point sites (BPS), and (BPS), and polypyrimidine channels (PPT). U1 snRNP recognized 5’ss, and SF1 bound BPS, U2AF2 and U2AF1, PPT, and 3’ss to form the E complex, respectively. U2 snRNP replaces SF1 and binds to BPS to form an A complex, which subsequently recruits U4, U5, and U6 triple snRNP complexes. The B complex is rearranged to form catalytically activated complex B, which is followed by two transesterification reactions catalyzing the eventual formation of mature mRNA and the intron Lariat. (B) Cis-regulatory elements in pre-mRNA interact with splicing factors to regulate the splicing process. SR proteins act as splicing activators and promote splicing by binding to ESEs and ISEs. HnRNPs act as repressors and inhibit binding to splice sites by interacting with ESSs and ISSs. (C) RNA splicing is composed of constitutive splicing and AS. AS including exon skipping, retention intron, alternative 5’ splicing, alternative 3’ splicing, mutually exclusive exon, alternative promoters, and alternative polyadenylation. Exons are represented by boxes, and introns by lines. Promoters are indicated by arrows, and polyadenylation sites are indicated by AAAA. This figure was drawn by Biorender

Back to article page