Document Detail

Transcriptional regulation of the p67phox gene: role of AP-1 in concert with myeloid-specific transcription factors.
MedLine Citation:
PMID:  11483614     Owner:  NLM     Status:  MEDLINE    
We have investigated the myeloid-specific transcriptional regulation of p67(phox), an essential component of phagocyte respiratory burst NADPH oxidase. Analysis was carried out on the p67(phox) 5'-flanking region from -3669 to -4 (relative to ATG), including the first exon and intron and part of the second exon. The construct extending from -985 to -4 produced the highest luciferase activity in myeloid HL-60 cells but was not active in HeLa or Jurkat cells, indicating myeloid-specific expression. Four active elements were identified: Sp1/Sp3 at -694, PU.1 at -289, AP-1 at -210, and PU.1/HAF1 at -182, the latter three being in the first intron. These cis elements bound their cognate transacting factors both in vitro and in vivo. Mutation of the Sp1, PU.1, or PU.1/HAF1 site each decreased promoter activity by 35-50%. Mutations in all three sites reduced promoter activity by 90%. However, mutation of the AP-1 site alone nearly abolished promoter activity. The AP-1 site bound Jun and Fos proteins from HL-60 cell nuclear extract. Co-expression with Jun B in AP-1-deficient cells increased promoter activity by 3-fold. These data show that full p67(phox) promoter activity requires cooperation between myeloid-specific and nonmyeloid transcription factors, with AP-1 being the most critical for function.
S L Li; A J Valente; L Wang; M J Gamez; R A Clark
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2001-08-01
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  276     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2001 Oct 
Date Detail:
Created Date:  2001-10-15     Completed Date:  2001-12-04     Revised Date:  2013-05-27    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  39368-78     Citation Subset:  IM    
Department of Medicine, University of Texas Health Science Center and South Texas Veterans Health Care System, Audie L. Murphy Division, San Antonio, Texas 78229-3900, USA.
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MeSH Terms
Base Sequence
Binding Sites
Cell Nucleus / metabolism
Cloning, Molecular
DNA-Binding Proteins / metabolism
Deoxyribonuclease I / metabolism
Gene Expression Regulation, Enzymologic*
HL-60 Cells
HeLa Cells
Jurkat Cells
Luciferases / metabolism
Molecular Sequence Data
Mutagenesis, Site-Directed
Phosphoproteins / genetics*,  metabolism*
Promoter Regions, Genetic*
Protein Binding
Protein Structure, Tertiary
Sp1 Transcription Factor / metabolism
Sp3 Transcription Factor
Transcription Factor AP-1 / genetics*,  metabolism*
Transcription Factors / metabolism
Transcription, Genetic*
Tumor Cells, Cultured
Grant Support
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Phosphoproteins; 0/SP3 protein, human; 0/Sp1 Transcription Factor; 0/Transcription Factor AP-1; 0/Transcription Factors; 0/neutrophil cytosol factor 67K; 148710-94-5/Sp3 Transcription Factor; EC 1.13.12.-/Luciferases; EC I

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

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