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Fig. 1 | Clinical Epigenetics

Fig. 1

From: Restoration of KMT2C/MLL3 in human colorectal cancer cells reinforces genome-wide H3K4me1 profiles and influences cell growth and gene expression

Fig. 1

Restored KMT2C expression in RKO and HCT116 CRC cells with corrected c.8390delA frameshift mutation. a Design of isogenic cell system, showing the amino acid sequence of KMT2C at the A9 repeat of exon 38 in KMT2C wild type (WT), c.8390delA (RKO and HCT116), and knock-in (KI) cells. The frameshift mutation in the repeat is corrected by insertion of one G base (green) in the middle of the repeat to generate KMT2CinsG clones. This restores the protein sequence, and the G stabilizes the repeat to prevent reintroduction of mutation in the repeat through mismatch repair deficiency. The sequence frame shift is shown in red for parental HCT116 and RKO cells. b Sequencing of the exon 38 A9 repeat in HCT116 KMT2CinsG KI2 clone cDNA to verify insertion of a G base (arrow) and expression of the corrected allele. c Level of KMT2C expression measured by RT-qPCR in parental cells and KMT2CinsG clones. TBP and HPRT1 were used as reference genes, and data were normalized to the respective parental cell line. Error bars, max and min relative quantity. Two tailed Student’s t-test; *P < 0.05, **P < 0.01, ***P < 0.001

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