| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
RI
Promoter Region Affecting Transcription Activity: A Possible Promoter-Dependent Mechanism for Association between FcRI and Atopy1
* Atopy (Allergy) Research Center, Departments of
Dermatology and
Immunology, Juntendo University School of Medicine, Tokyo, Japan;
Advanced Research Laboratory, Hanno Research Center, Taiho Pharmaceutical Co. Ltd., Saitama, Japan;
¶ Biotechnology Research Center, University of Tokyo, Tokyo, Japan;
|| Department of Pediatrics, Yamaguchi University School of Medicine, Yamaguchi, Japan;
# Department of Dermatology, Tokyo Medical University, Tokyo, Japan; and
** Department of Immunology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan
The 
subunit of the high-affinity IgE receptor (Fc
RI) plays an important role in IgE-mediated allergic reactions as an amplifier for cell surface expression and signal transduction of FcRI. FcRI is presumed to be one of the genes linked with atopic diseases. However, the validity of the associations previously found between single nucleotide polymorphisms (SNPs) in FcRI and atopic diseases is questionable. In the present study, we found correlation between the SNP of FcRI at +6960A/G, resulting in a Glu237Gly amino acid substitution, and the cell surface expression level of FcRI on blood basophils, although it has been shown that the Glu237Gly mutation itself does not affect the surface expression or function of FcRI. We additionally found four SNPs in the promoter region of FcRI, among which –426T/C and –654C/T were tightly linked with +6960A/G. Reporter plasmids carrying the –426C and –654T promoter displayed higher transcriptional activity than those carrying the –426T and –654C promoter. We found that transcription factor YY1 preferentially bound and transactivated the –654T promoter. Furthermore, expression of FcRI -chain mRNA in basophils from individuals who have the minor heterozygous genotype was significantly higher than that of the major homozygous genotype. These results suggest that the SNPs in the FcRI promoter are causally linked with atopy via regulation of FcRI expression.
This article has been cited by other articles:
|
|
 |
|
  S. Kanada, N. Nakano, D. P. Potaczek, K. Maeda, N. Shimokawa, Y. Niwa, T. Fukai, M. Sanak, A. Szczeklik, H. Yagita, et al. Two Different Transcription Factors Discriminate the -315C>T Polymorphism of the Fc{epsilon}RI{alpha} Gene: Binding of Sp1 to -315C and of a High Mobility Group-Related Molecule to -315T J. Immunol., June 15, 2008; 180(12): 8204 - 8210. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. S. Gounni The high-affinity IgE receptor (Fc{epsilon}RI): a critical regulator of airway smooth muscle cells? Am J Physiol Lung Cell Mol Physiol, September 1, 2006; 291(3): L312 - L321. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Nishiyama, T. Ito, M. Nishiyama, S. Masaki, K. Maeda, N. Nakano, W. Ng, K. Fukuyama, M. Yamamoto, K. Okumura, et al. GATA-1 is required for expression of Fc{varepsilon}RI on mast cells: analysis of mast cells derived from GATA-1 knockdown mouse bone marrow Int. Immunol., July 1, 2005; 17(7): 847 - 856. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. MacGLASHAN JR. IgE and Fc{epsilon}RI Regulation Ann. N.Y. Acad. Sci., June 1, 2005; 1050(1): 73 - 88. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Ito, C. Nishiyama, M. Nishiyama, H. Matsuda, K. Maeda, Y. Akizawa, R. Tsuboi, K. Okumura, and H. Ogawa Mast Cells Acquire Monocyte-Specific Gene Expression and Monocyte-Like Morphology by Overproduction of PU.1 J. Immunol., January 1, 2005; 174(1): 376 - 383. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
