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. 2014 Apr 15;28(8):829–834. doi: 10.1101/gad.235499.113

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© 2014 Zhang et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 5. — Hhex maintains δ-cell number through transcriptional up-regulation of Sst rather than affecting apoptosis. (A) Ectopic expression of HHEX is sufficient to induce Sst expression in MIN6 cells transfected with a Myc-tagged HHEX expression plasmid (n = 3). (B) Overexpression of HHEX in HeLa cells fails to activate Sst (n = 3). (C) ChIP using an anti-Myc 9E10 antibody was performed on Myc-tagged HHEX-expressing MIN6 cells followed by qPCR evaluation of enrichment at three putative binding sites of Hhex within the Sst promoter. Data are presented as the fold enrichment of the target amplicon in ChIP DNA compared with input DNA (n = 2 or 3). (D) Dual-luciferase reporter assays were conducted in MIN6 cells transfected with reporter constructs containing the intact (pGL3-Sst WT) or mutated (pGL3-Sst MT) proximal promoter of Sst or the basic vector pGL3 (n = 3). Data are represented as mean ± SEM. (*) P < 0.05; (***) P < 0.001; (ns) not significant. See also Supplemental Figure S3.