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Most mammalian protein coding genes are subject to alternative cleavage and polyadenylation (APA), which can generate distinct mRNA 3'UTRs with differing regulatory potential. Although this process has been intensely studied in recent years, it remains unclear how and to what extent cleavage site selection is regulated under different physiological conditions. The cleavage factor Im (CFIm) complex is a core component of the mammalian cleavage machinery, and the observation that its depletion causes transcriptome-wide changes in cleavage site use makes it a key candidate regulator of APA. This review aims to summarize current knowledge of the CFIm complex, and explores the evidence surrounding its potential contribution to regulation of APA.

Original publication




Journal article


Biochem Soc Trans

Publication Date





1051 - 1057


cancer, cell proliferation, gene expression, mRNA biogenesis, polyadenylation, post-transcriptional regulation of gene expression, 3' Untranslated Regions, Alternative Splicing, Animals, Base Sequence, Binding Sites, Humans, Models, Genetic, Polyadenylation, Transcriptome, mRNA Cleavage and Polyadenylation Factors