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Unique aspects of transcriptional regulation in neurons – nuances in NFκB and Sp1-related factors

Xianrong R Mao1 email, Andréa M Moerman-Herzog2 email, Yuzhi Chen2,3 email and Steven W Barger2,3,4 email

Department of Anesthesiology, Washington University School of Medicine, St Louis MO 63110, USA

Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock AR 72205, USA

Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock AR 72205, USA

Geriatric Research Education and Clinical Center, Central Arkansas Veterans Healthcare System, Little Rock AR 72205, USA

author email corresponding author email

Journal of Neuroinflammation 2009, 6:16doi:10.1186/1742-2094-6-16

Published: 18 May 2009

Abstract

The unique physiology and function of neurons create differences in their cellular physiology, including their regulation of gene expression. We began several years ago exploring the relationships between the NFκB transcription factor, neuronal survival, and glutamate receptor activation in telencephalic neurons. These studies led us to conclude that this population of cells is nearly incapable of activating the NFκB that is nonetheless expressed at reasonable levels. A subset of the κB cis elements are instead bound by members of the Sp1 family in neurons. Also surprising was our discovery that Sp1 itself, typically described as ubiquitous, is severely restricted in expression within forebrain neurons; Sp4 seems to be substituted during neuronal differentiation. These findings and their implications for neuronal differentiation – as well as potential dedifferentiation during degenerative processes – are discussed here.


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