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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: J Immunol. 2015 Oct 1;195(7):2963–2971. doi: 10.4049/jimmunol.1500756

Figure 2. Post-transcriptional regulation of the 3′ UTR and its implications for immune disorders.

Figure 2

Insertion (INS) or deletion (DEL) mutations in the 3′ UTR of the gene could create or destroy binding sites for regulators such as RNA binding proteins (RBPs) and microRNAs (miRNAs). This could lead increased or decreased mRNA stability and protein levels. Likewise, single nucleotide polymorphisms (SNPs) in the 3′ UTR can create new alternative polyadenylation signals or destroy poly(A) signals altering the length of the 3′ UTR affecting the stability of mRNA. Elimination of interaction motifs/sequences for RBPs and miRNAs leads to increased mRNA stability and protein levels. These SNPs affect post-transcriptional control of genes involved in innate and adaptive immunity. Hence, carriers of the risk or protective alleles can be more likely to develop or resist immune disorders like immunodeficiency, autoimmunity or cancer.