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. 2017 Dec 14;46(4):2030–2044. doi: 10.1093/nar/gkx1255

Figure 8.

Figure 8.

Model: PCBP1 controls exon 5 splicing of the human CKD2 gene transcript via interaction with a recently evolved C-rich PPT. The regions of the mouse and human CDK2 genes that encompass exon 5 and its two flanking exons are shown (not drawn to scale). U: U-rich PPT; C: C-rich PPT. U2AF65 and PCBP1 are RNA binding proteins interacting with U-rich PPT, C-rich PPT, respectively. The mouse U-rich PPT interacts with U2AF65, the canonical PPT binding protein, to ensure that mouse CDK2 exon 4 is spliced to exon 5 constitutively. Human C-rich PPT interacts with PCBP1 proteins to regulate the inclusion of exon 5 in the hCDK2 transcript. The efficiency of AS event is likely to be impacted by the PCBP1 availability and activity (level and modification). When PCBP1 is available, it binds to the C-rich PPT resulting in the inclusion of exon 5. When PCBP1 level/activity is reduced in the cells, exon 5 will be skipped and CDK2 protein expression will be markedly diminished (downward arrow). By this mechanism, the cell cycle can be modulated in response to external or internal cues, through alterations CDK2 expression.