3′ UTR lengthening as a novel mechanism in regulating cellular senescence

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Figure 5.
Figure 5.

Working model for APA as a new mechanism in regulating cellular senescence. Genes, such as RRAS2, favor distal pA site usage during senescence, leading to 3′ UTR lengthening. Splicing factor TRA2B bound to its core cis-element “AGAA” located in the alternative 3′ UTR of RRAS2 and repressed RRAS2 protein production, thereby leading to senescence-associated phenotypes.

This Article

  1. Published in Advance February 12, 2018, doi: 10.1101/gr.224451.117 Genome Res. 28: 285-294

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