Regulation of CEP131 gene expression by SP1

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Title
Regulation of CEP131 gene expression by SP1
Author(s)
P T T Huong; Nak Kyun SoungJae-Hyuk JangHyunjoo Cha; K Sakchaisri; Sun Ok Kim; J M Jang; K E Kim; K S Lee; Y T Kwon; R L Erikson; Jong Seog AhnBo Yeon Kim
Bibliographic Citation
Gene, vol. 513, no. 1, pp. 75-81
Publication Year
2013
Abstract
Centrosomal proteins play important roles in cell cycle. Among them, the centrosomal protein of 131. kDa (CEP131) has been reported as a critical factor for cilia formation which is related with development, signaling, and various diseases, the malfunction of cilia leading to cancer. Specificity protein 1 (SP1), known as a centrosome regulator, is an essential transcription factor regulating the genes involved in multiple cellular processes such as cell cycle, apoptosis, and DNA damages. In this study, we explored the crucial role of SP1 in the regulation of CEP131 gene transcription. A deletion analysis of the CEP131 promoter region revealed dominant promoter elements within the sequence between - 400. bp and - 200. bp, which contained consensus binding sites for SP1. Electrophoretic mobility shift assay (EMSA) and chromatin immuno-precipitation (ChIP) assay further confirmed the direct binding of SP1 to the CEP131 promoter. On the other hand, CEP131 transcription could be inhibited by mithramycin (a GC-rich region inhibitor), but exogenous expression of SP1 could increase CEP131 expression as evidenced by a reporter gene assay. In addition, mutation of several SP1 binding sites revealed four SP1 binding sites at - 244/- 225, - 258/- 239, - 304/- 283 and - 323/- 304 that strongly affect CEP131 expression. Hence, it is suggested that SP1 is a pivotal transcription factor for the regulation of CEP131 expression, consequently leading the control of centrosome functions.
Keyword
Transcription factor SP1CentrosomeCEP131CPAPDHFRPARP-1SP1
ISSN
0378-1119
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.gene.2012.10.074
Type
Article
Appears in Collections:
Ochang Branch Institute > Chemical Biology Research Center > 1. Journal Articles
Ochang Branch Institute > Nucleic Acid Therapeutics Research Center > 1. Journal Articles
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