|
|
 Previous Article | Table of Contents | Next Article 
Blood, Vol. 93 No. 10 (May 15), 1999:
pp. 3512-3520
Elf-1 and PU.1 Induce Expression of gp91phox Via a
Promoter Element Mutated in a Subset of Chronic Granulomatous
Disease Patients
Kui Shin Voo and
David G. Skalnik
From the Herman B Wells Center for Pediatric Research, Section of
Pediatric Hematology/Oncology, Department of Pediatrics, Indiana
University School of Medicine, Indianapolis, IN.
The cytochrome b heavy chain (gp91phox) is the
redox center of the NADPH-oxidase and is highly expressed in mature
myeloid cells. Point mutations at  57, 55, 53, and 52 bp of
the gp91phox promoter have been detected in
patients with chronic granulomatous disease (CGD; Newburger et al,
J Clin Invest 94:1205, 1994; and Suzuki et al, Proc
Natl Acad Sci USA 95:6085, 1998). We report that Elf-1 and PU.1,
ets family members highly expressed in myeloid cells, bind to
this promoter element. Either factor trans-activates the 102 to
+12 bp gp91phox promoter when overexpressed in
nonhematopoietic HeLa cells or the PLB985 myeloid cell line. However,
no synergy of gp91phox promoter activation occurs
when both Elf-1 and PU.1 are overexpressed. Introduction of the 57
bp or 55 bp CGD mutations into the gp91phox
promoter significantly reduces the binding affinity of Elf-1 and PU.1
and also reduces the ability of these factors to trans-activate the
promoter. These results indicate that Elf-1 and PU.1 contribute to
directing the lineage-restricted expression of the
gp91phox gene in phagocytes and that failure of
these factors to effectively interact with this promoter results in CGD.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
K. Bedard and K.-H. Krause
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Physiol Rev,
January 1, 2007;
87(1):
245 - 313.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Shimokawa and C. Ra
C/EBP{alpha} functionally and physically interacts with GABP to activate the human myeloid IgA Fc receptor (Fc{alpha}R, CD89) gene promoter
Blood,
October 1, 2005;
106(7):
2534 - 2542.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Thomas, S. Samanta, C. Wu, N. Berliner, and E. Fikrig
Anaplasma phagocytophilum Modulates gp91phox Gene Expression through Altered Interferon Regulatory Factor 1 and PU.1 Levels and Binding of CCAAT Displacement Protein
Infect. Immun.,
January 1, 2005;
73(1):
208 - 218.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. T. Quinn and K. A. Gauss
Structure and regulation of the neutrophil respiratory burst oxidase: comparison with nonphagocyte oxidases
J. Leukoc. Biol.,
October 1, 2004;
76(4):
760 - 781.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Mazzi, M. Donini, D. Margotto, F. Wientjes, and S. Dusi
IFN-{gamma} Induces gp91phox Expression in Human Monocytes via Protein Kinase C-Dependent Phosphorylation of PU.1
J. Immunol.,
April 15, 2004;
172(8):
4941 - 4947.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. D. Bjerregaard, J. Jurlander, P. Klausen, N. Borregaard, and J. B. Cowland
The in vivo profile of transcription factors during neutrophil differentiation in human bone marrow
Blood,
June 1, 2003;
101(11):
4322 - 4332.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S.-L. Li, A. J. Valente, M. Qiang, W. Schlegel, M. Gamez, and R. A. Clark
Multiple PU.1 sites cooperate in the regulation of p40phox transcription during granulocytic differentiation of myeloid cells
Blood,
May 29, 2002;
99(12):
4578 - 4587.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Kumatori, D. Yang, S. Suzuki, and M. Nakamura
Cooperation of STAT-1 and IRF-1 in Interferon-gamma -induced Transcription of the gp91phox Gene
J. Biol. Chem.,
March 8, 2002;
277(11):
9103 - 9111.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. A. Gauss, P. L. Bunger, and M. T. Quinn
AP-1 is essential for p67phox promoter activity
J. Leukoc. Biol.,
January 1, 2002;
71(1):
163 - 172.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S.-L. Li, A. J. Valente, L. Wang, M. J. Gamez, and R. A. Clark
Transcriptional Regulation of the p67phox Gene. ROLE OF AP-1 IN CONCERT WITH MYELOID-SPECIFIC TRANSCRIPTION FACTORS
J. Biol. Chem.,
October 12, 2001;
276(42):
39368 - 39378.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Gorlach, R. P. Brandes, K. Nguyen, M. Amidi, F. Dehghani, and R. Busse
A gp91phox Containing NADPH Oxidase Selectively Expressed in Endothelial Cells Is a Major Source of Oxygen Radical Generation in the Arterial Wall
Circ. Res.,
July 7, 2000;
87(1):
26 - 32.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Catt, S. Hawkins, A. Roman, W. Luo, and D. G. Skalnik
Overexpression of CCAAT Displacement Protein Represses the Promiscuously Active Proximal gp91phox Promoter
Blood,
November 1, 1999;
94(9):
3151 - 3160.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. M. Jacobsen and D. G. Skalnik
YY1 Binds Five cis-Elements and Trans-activates the Myeloid Cell-restricted gp91phox Promoter
J. Biol. Chem.,
October 15, 1999;
274(42):
29984 - 29993.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. M. Hawkins, T. Kohwi-Shigematsu, and D. G. Skalnik
The Matrix Attachment Region-binding Protein SATB1 Interacts with Multiple Elements within the gp91phox Promoter and Is Down-regulated during Myeloid Differentiation
J. Biol. Chem.,
November 21, 2001;
276(48):
44472 - 44480.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
