Figure 1
Figure 1. Establishment and characterization of iPSCs. (A) Sequencing of the NLRP3 1709 A > G mutation (Y570C) in fibroblasts (FIBRO), mutant iPSCs (M1), and wild-type iPSCs (W1) in patient 1. (B) The morphology of the mutant and wild-type iPSCs. (C) NANOG expression in CINCA iPSCs, control iPSCs (B7), control ESCs (khES3), fibroblasts (FIBRO), and fibroblasts transduced with 4 factors (FIBRO4F) normalized to GAPDH. n = 3. (D) A quantitative RT-PCR assay for the expression of OCT3/4, SOX2, KLF4, and cMYC in iPSCs. One primer set detects only the transgene (in black), and the other primer set detects both the transgene and endogenous gene (in white). n = 3. (E) Retroviral transgene integration analyses. Southern blot analyses were performed with DIG-labeled DNA probes against c-MYC. The parental fibroblasts carried a band in common with all of the iPSC lines (arrow). (F) A teratoma derived from a mutant iPSC clone, M1. Scale bars represent 100 μm. Data are mean ± SEM.

Establishment and characterization of iPSCs. (A) Sequencing of the NLRP3 1709 A > G mutation (Y570C) in fibroblasts (FIBRO), mutant iPSCs (M1), and wild-type iPSCs (W1) in patient 1. (B) The morphology of the mutant and wild-type iPSCs. (C) NANOG expression in CINCA iPSCs, control iPSCs (B7), control ESCs (khES3), fibroblasts (FIBRO), and fibroblasts transduced with 4 factors (FIBRO4F) normalized to GAPDH. n = 3. (D) A quantitative RT-PCR assay for the expression of OCT3/4, SOX2, KLF4, and cMYC in iPSCs. One primer set detects only the transgene (in black), and the other primer set detects both the transgene and endogenous gene (in white). n = 3. (E) Retroviral transgene integration analyses. Southern blot analyses were performed with DIG-labeled DNA probes against c-MYC. The parental fibroblasts carried a band in common with all of the iPSC lines (arrow). (F) A teratoma derived from a mutant iPSC clone, M1. Scale bars represent 100 μm. Data are mean ± SEM.

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