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Anderson, A.A., Treves, S., Biral, D., Betto, R., Sandonà, D., Ronjat, M. and Zorzato, F. (2003) The novel skeletal muscle sarcoplasmic reticulum JP-45 protein. Molecular cloning, tissue distribution, developmental expression, and interaction with alpha 1.1 subunit of the voltagegated calcium channel. Journal of Biological Chemistry, 278, 39987-39989. doi:10.1074/jbc.M305016200

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• TITLE: Interaction between the Wilms tumour factor-1 element in the promoter of Amh and a downstream enhancer is required for a strong expression of the gene in pre-pubertal sertoli cells

  AUTHORS: David W. Dresser

  KEYWORDS: Mouse Cell Lines; In Vitro; Amh Promoter; SMAT; Pre-Pubertal Sertoli; Downstream Enhancer; Wilms Tumour Factor Element

  JOURNAL NAME: American Journal of Molecular Biology, Vol.3 No.3, July 17, 2013

  ABSTRACT: Amh (anti-Müllerian hormone) is a single copy gene which is expressed strongly in Sertoli cells in the foetal testis and participates in the onset of sexual differentiation. Its promoter driving the expression of a reporter gene (d2EGFP) has been used to analyse the role of certain defined putative elements and a downstream enhancer element in gene expression. These experiments were carried out in vitro using a line of pre-pubertal mouse Sertoli cells, transienly transfected with circular DNA constructs with variously mutated promoter elements. A downstream enhancer element, situated immediately 3’ of the polyadenylation (PA) signal for Amh, has been inserted in an equivalent position in the d2EGFP construct. When the Amh promoter is unmodified, the downstream enhancer (DE) is positively associated with a large increase in EGFP expression. This is at least partly the consequence of an increased rate of expression by individual cells. Experiments using variously truncated Amh promoters indicate that an upstream region (-214 to -336) may play a minor role in facilitating enhancement. However mutation of the Wilms tumour factor-1 element, situated between the tata box and the start of translation, results in an almost complete suppression of enhancement.