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. 2019 Aug 22;4(16):e126457. doi: 10.1172/jci.insight.126457

Figure 3. Defects in B55β upregulation are not caused by expansion or contraction of the CAG trinucleotide repeat in PPP2R2B.

Figure 3

(A) Schematic representation of the genomic location of the first exon and 5′ untranslated region (UTR) of PPP2R2B. The location of the CAG repeats and of the primers used to quantify the number of repeats in each individual are indicated by an inverted triangle and by arrows, respectively. (B) The distribution of allele length in HDs and patients with SLE and RA is shown (HD n = 20; SLE n = 20; RA n = 21). (C) CAG repeat length in individuals who exhibited normal versus abolished upregulation of B55β during cytokine withdrawal was compared (normal B55β induction n = 21; deficient B55β induction n = 26).