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. 2014 Oct 15;28(20):2248–2260. doi: 10.1101/gad.245787.114

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© 2014 Di Giammartino et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 7. — Model for RBBP6-mediated regulation of 3′ processing. (A) RBBP6 iso1 competes with iso3 in binding to CstF64. When iso1 is up-regulated and/or iso3 is down-regulated, such as in cancer cells, iso1 can bind to CstF64, and pre-mRNA 3′ processing functions properly; when the opposite is true (for example, after knockdown of iso1 or overexpression of iso3), 3′ cleavage is inhibited by binding of iso3 to CstF64, resulting in down-regulation of gene expression, especially of ARE-containing transcripts. (B) RBBP6 affects APA and gene expression. In genes with two or more APA sites, when RBBP6 levels are low and/or iso3 levels are high, the more distant and typically strongest poly(A) site will be used, resulting in 3′ UTR lengthening. However, if there is only a single poly(A) site or if the distal site is not strong enough, then the pre-mRNA will not be cleaved, and failure to process the RNA will lead to its degradation by the exosome.