Fig. 7. Glucose decreases the transcriptional activity of the human Cx36 promoter through a CRE. (A) Progressive deletions of the human Cx36 promoter were transfected into INS-1 cells. After transfection, cells were incubated at 2 mM or 20 mM glucose. The –1079 to –316 region of the Cx36 promoter drives glucose responsiveness. The mutation of a CRE (pGL3-1079m) located in this region abolished the inhibitory effect of glucose on the luciferase activity. Results are means ± s.e.m. of four experiments performed in triplicate. Luciferase activities were normalized using the pRLSV40renilla construct. ^*, P<0.05. NRSE, neuron-restrictive silencing element. (B) Alignments of CREs: the TGACG core region (bold) of the consensus CRE is 100% conserved between the three species. HIP CRE1, human insulin promoter CRE 1; HIP CRE 2, human insulin promoter CRE 2; RIP1 CRE, rat insulin promoter 1 CRE.