Transcription factor Sp1 regulates basal transcription of the human DRG2 gene
Autor: | Hong Kyung Kim, Wha Ja Cho, Myoung Seok Ko, Hyo Jeong Kim, Byung Ju Lee, Jeong Woo Park, Seon Ho Lee |
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Rok vydání: | 2011 |
Předmět: |
Transcription
Genetic Cell Survival Sp1 Transcription Factor DNA Mutational Analysis Molecular Sequence Data Biophysics E-box Biology Biochemistry Sp3 transcription factor GTP-Binding Proteins Structural Biology Genetics Humans Gene Silencing Promoter Regions Genetic Enhancer Molecular Biology Sequence Deletion Regulation of gene expression Sp1 transcription factor Binding Sites Base Sequence General transcription factor Promoter TCF4 Molecular biology Gene Expression Regulation Mutation K562 Cells Protein Binding |
Zdroj: | Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms. 1809:184-190 |
ISSN: | 1874-9399 |
DOI: | 10.1016/j.bbagrm.2011.01.004 |
Popis: | Developmentally regulated GTP-binding protein 2 (DRG2) is an evolutionarily conserved GTP-binding protein. DRG2 mRNA expression has been confirmed in many animal and human tissues. DRG2 is thought to play an essential role in the control of cell growth and differentiation. However, transcriptional regulation of DRG2 is largely unknown. To investigate the mechanisms controlling DRG2 expression, we cloned 1509bp of the 5'-flanking sequence of this gene. Deletion analysis showed that the region between -113 and -70 is essential for the basal level expression of the DRG2 gene in K562 human erythroleukemic cells. Mutation of a putative stimulating protein 1 (Sp1) regulatory site located at position -108 resulted in a significant decline in DRG2 promoter activity. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis revealed that Sp1 binds to this site. Knockdown of Sp1 expression using siRNA inhibited the promoter activation as well as the endogenous DRG2 transcriptional level. Taken together, these results demonstrate that basal expression level of DRG2 is regulated by the Sp1 transcription factor. |
Databáze: | OpenAIRE |
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