Transcriptional control of the neuronal nicotinic acetylcholine receptor gene cluster by the β43′ enhancer, Sp1, SCIP and ETS transcription factors

被引：9

作者：

Deneris, ES ^{[1
]}

Francis, N ^{[1
]}

McDonough, J ^{[1
]}

Fyodorov, D ^{[1
]}

Miller, T ^{[1
]}

Yang, XD ^{[1
]}

机构：

[1] Case Western Reserve Univ, Sch Med, Dept Neurosci, Cleveland, OH 44106 USA

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2000年 / 393卷 / 1-3期

关键词：

nicotinic receptor; transcription; enhancer; promoter; neuron;

D O I：

10.1016/S0014-2999(99)00883-3

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Receptors assembled from the products of a neuronal beta 4 alpha 3 alpha 5 NAChR gene cluster depend on these genes being coordinately regulated in particular populations of neurons. Little is known, however, about the transcriptional mechanisms that are likely to underlie their co-expression in correct neuronal cell types. We have identified several regulatory elements and transcription factors that influence transcription of the alpha 3 and beta 4 genes. The promoters of these genes appear to contain a common cis element that binds Sp1 transcription factors. They can be activated by the POU-domain factor SCIP and activation does not require SCIP binding sites. Between these two promoters is a cell type specific enhancer called beta 43'. This enhancer has little activity in non-neuronal cells and is preferentially active in particular populations of central neurons. The clustered genes are potential targets of ETS factors as the ETS domain factor, Pet-1 can activate beta 43'-dependent transcription. The neuron-selective properties of beta 43' and its location suggest that it is a component of the cia regulatory information required to control expression of the beta 4 and alpha 3 genes in specific populations of neurons. (C) 2000 Elsevier Science B.V. All rights reserved.

引用

页码：69 / 74

页数：6