Document Detail

EGR1, EGR2, and EGR3 activate the expression of their coregulator NAB2 establishing a negative feedback loop in cells of neuroectodermal and epithelial origin.
MedLine Citation:
PMID:  20506119     Owner:  NLM     Status:  MEDLINE    
The inducible zinc finger transcription factors EGR1, EGR2, and EGR3 regulate the expression of numerous genes involved in differentiation, growth, and response to extracellular signals. Their activity is modulated in part through NAB2 which is induced by the same stimuli. In melanoma and carcinoma cells EGR1 activates NAB2 expression. In T lymphocytes EGR2 and EGR3 have been shown to inhibit NAB2 expression. Therefore, we investigated the influence of EGR2 and EGR3 on NAB2 expression in melanoma and carcinoma cells. Here, we show that like EGR1, EGR2 and EGR3 induced NAB2 expression in these cells. EGR1 and EGR3 act in concert on the NAB2 promoter and are more potent activators of NAB2 transcription than EGR2. EGR1-, EGR2-, and EGR3-induced NAB2 promoter activity is mediated through similar cis-regulatory elements and the activation by each EGR is repressed by NAB2. Kinetic studies suggest that induction of EGR1 leads to low NAB2 expression, while EGR2 and EGR3 are necessary for maximal and sustained expression. As already shown for EGR1, reduction of EGR2 or EGR3 expression by siRNAs reduced endogenous NAB2 levels. Depletion of EGR3 also resulted in a reduction of EGR2 levels confirming EGR2 as a target gene of EGR3. Our results suggest that in many cells of neuroectodermal and epithelial origin EGR1, EGR2, and EGR3 activate NAB2 transcription which is in turn repressed by NAB2, thus establishing a negative feedback loop. This points to a complex relationship between the EGR factors and NAB2 expression likely depending on the cellular context.
Joerg Kumbrink; Kathrin H Kirsch; Judith P Johnson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  111     ISSN:  1097-4644     ISO Abbreviation:  J. Cell. Biochem.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-30     Completed Date:  2011-02-14     Revised Date:  2011-09-13    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  207-17     Citation Subset:  IM    
Copyright Information:
(c) 2010 Wiley-Liss, Inc.
Institute for Immunology, University of Munich, Munich 80336, Germany.
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MeSH Terms
Cell Line, Tumor
Early Growth Response Protein 1 / genetics,  metabolism*
Early Growth Response Protein 2 / genetics,  metabolism*
Early Growth Response Protein 3 / genetics,  metabolism*
Epithelial Cells / cytology,  physiology*
Feedback, Physiological / physiology*
Gene Expression Regulation
Neural Plate / cytology*
Promoter Regions, Genetic
RNA, Small Interfering / genetics,  metabolism
Repressor Proteins / genetics,  metabolism*
T-Lymphocytes / cytology,  physiology
Transcription, Genetic
Grant Support
CA106468/CA/NCI NIH HHS; R01 CA106468-05/CA/NCI NIH HHS
Reg. No./Substance:
0/EGR1 protein, human; 0/EGR2 protein, human; 0/EGR3 protein, human; 0/Early Growth Response Protein 1; 0/Early Growth Response Protein 2; 0/NAB2 protein, human; 0/RNA, Small Interfering; 0/Repressor Proteins; 144516-98-3/Early Growth Response Protein 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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