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Experiment performed as described in Fig

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We then mutated these potential binding motifs in the OXTR full length (pOXTR-2000) reporter construct, and the reporter assay showed that hyperglycemia-induced reporter activation disappeared in two of the ERE mutation constructs (located at 1005 and 944, respectively, marked in green, see Figure 2B), indicating that hyperglycemia mediates OXTR suppression through the ERE binding motif on the OXTR promoter (see Figure 2C)