Involvement of PU.1 in Mast Cell/Basophil-Specific Function of the Human <i>IL1RL1/ST2</i> Promoter
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- Baba Yosuke
- Atopy (Allergy) Research Center, Juntendo University School of Medicine Department of Pediatrics and Adolescence Medicine, Juntendo University School of Medicine
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- Maeda Keiko
- Atopy (Allergy) Research Center, Juntendo University School of Medicine
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- Yashiro Takuya
- Atopy (Allergy) Research Center, Juntendo University School of Medicine
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- Inage Eisuke
- Atopy (Allergy) Research Center, Juntendo University School of Medicine Department of Pediatrics and Adolescence Medicine, Juntendo University School of Medicine
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- Niyonsaba François
- Atopy (Allergy) Research Center, Juntendo University School of Medicine
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- Hara Mutsuko
- Atopy (Allergy) Research Center, Juntendo University School of Medicine
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- Suzuki Ryuyo
- Department of Pediatrics and Adolescence Medicine, Juntendo University School of Medicine
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- Ohtsuka Yoshikazu
- Department of Pediatrics and Adolescence Medicine, Juntendo University School of Medicine
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- Shimizu Toshiaki
- Atopy (Allergy) Research Center, Juntendo University School of Medicine Department of Pediatrics and Adolescence Medicine, Juntendo University School of Medicine
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- Ogawa Hideoki
- Atopy (Allergy) Research Center, Juntendo University School of Medicine
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- Okumura Ko
- Atopy (Allergy) Research Center, Juntendo University School of Medicine
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- Nishiyama Chiharu
- Atopy (Allergy) Research Center, Juntendo University School of Medicine
Bibliographic Information
- Other Title
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- Involvement of PU.1 in Mast Cell/Basophil-Specific Function of the Human IL1RL1/ST2 Promoter
- Involvement of PU. 1 in mast cell/basophil-specific function of the human IL1RLI/ST2 promoter
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Abstract
Background: The human IL1RL1/ST2 gene encodes IL33 receptor. Recently, IL33 has been recognized as a key molecule for the development of Th2 response. Although mast cells and basophils are major targets of IL33 and play important roles in IL33-mediated Th2-type immune responses, the expression mechanism of ST2 in mast cells and basophils is largely unknown. In the present study, we analyzed regulation mechanism of the human ST2 promoter in the human mast cell line LAD2 and basophilic cell line KU812.<br> Methods: Promoter activity was determined by reporter assay with plasmids carrying the wild-type ST2 promoter obtained from human genomic DNA and its mutant. The transcription factor binding to the identified cis-element was identified by an electrophoretic mobility shift assay (EMSA). The effect of candidate transcription factor on ST2 expression was confirmed by analyzing ST2 mRNA level in siRNA-introduced cells.<br> Results: Reporter assay demonstrated that a cis-element of typical Ets-family binding sequence was critical for promoter activity in LAD2 and KU812. An Ets-family transcription factor PU.1 bound to this element in an EMSA. When PU.1 expression was suppressed by siRNA, ST2 mRNA level was significantly reduced in KU812.<br> Conclusions: These observations indicated that PU.1 positively regulates the ST2 promoter as a transcription factor that directly transactivates the ST2 promoter via Ets-family-related cis-element in mast cells and basophils.<br>
Journal
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- Allergology International
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Allergology International 61 (3), 461-467, 2012
Japanese Society of Allergology