Transcription factors involve in expression of allergic-related genes

转录因子参与过敏相关基因的表达

• 批准号: 17607012
• 负责人: NISHIYAMA Chiharu
• 金额: $ 2.3万
• 依托单位: JUNTENDO UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2005
• 资助国家: 日本
• 起止时间: 2005 至 2006
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17607012/
• 关键词: PU.1; GATA-1; Mast cells; Dendritic cells; IgE receptor; Allergy; Single Nucleotide Polymorphism; Hematopoietic stem cells; FOG-1

I am studying the cell type-specific gene expression mechanism in mast cells, which play important roles in IgE-mediated allergic reaction and are main target of anti-allergic drugs, because the suppression of mast cell-specific genes (especially FceRI) may provide novel tools for the prevention or treatment of allergic diseases. Previously, the study of transcriptional regulation mechanism of FcERI α-chain gene revealed that cooperation between transcription factors GATA-1 and PU.1 is one of mast cell-specific gene regulation mechanism (Nishiyama, J. Immunol. 2002). We also found that repression of GATA-1-dependent transactivation by cofactor FOG-1 causes mast cell-specific gene expression through the analysis of FcERI β-chain gene promoter in the recent study (Maeda, Blood 2006). Involvement of GATA-1 in FcERI expression was confirmed by the analysis of mast cells derived from GATA-1 knockdown mice (kindly provided by Prof. Masayuki Yamamoto, Tsukuba University). In addition, we reported that the expression level of PU.1 not only regulates monocyte-specific genes, but also determines cell fates including morphology and function (Ito, J. Immunol. 2005). Furthermore, we found that mast cells are a crucial source of functional IL-12 during the study of a transcription factor IRF-8, which forms heterodimer with PU.1 (Nakano, Blood, 2007). I was awarded the award for young scientists from Japan Society for Bioscience, Biotechnology, and Agrochemistry in 2005 and from Japanese Society for Allergology in 2006 through the above-mentioned studies.

我正在研究肥大细胞中类型的基因机制，因为抑制肥大细胞特异性基因（尤其是FCERI）可能会为治疗过敏性疾病的治疗提供新的工具。 1和pu.1是肥大细胞特异性基因调节机制之一（Nishiyama，J。Immunol。2002）。链基因在最近的研究中（MAEDA，血液，2006年）。 PU .1不是Onley单核细胞特异性基因，但也决定了包括和功能在内的细胞命运（ITO，J。Immunol。2005），我们发现肥大细胞是转录因子IRF的功能性IL-12的至关重要来源。 -8，与PU.1形成异二聚体（Nakano，Blood，2007年）。

项目成果

Transcriptional regulation of ATP2C1 gene by Sp1 and YY1 and reduced function of its promoter in Hailey-Hailey disease keratinocytes

• DOI: 10.1111/j.0022-202x.2005.23748.x
• 发表时间: 2005-06-01
• 期刊: JOURNAL OF INVESTIGATIVE DERMATOLOGY
• 影响因子: 6.5
• 作者: Kawada, H;Nishiyama, C;Ogawa, H
• 通讯作者: Ogawa, H

Involvement of mast cells in IL-12/23 p40 production is essential for survival from polvmicrobial infections.

肥大细胞参与 IL-12/23 p40 的产生对于多微生物感染的生存至关重要。

• 发表时间: 2007
• 期刊: Blood (in press)
• 作者: Nakano;N.;Nishiyama.C.;Kanada;S.;Niwa;Y.;Shimokawa;N.;Ushio;H.;Nishiyama;M.;Okumura;K.;Ogawa;H.
• 通讯作者: H.

Inhibitory effect of polyphenol-enriched apple extracts on mast cell degranulation in vitro targeting the binding between IgE and FcεRI

• DOI: 10.1271/bbb.69.1974
• 发表时间: 2005-10-01
• 期刊: BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
• 影响因子: 1.6
• 作者: Tokura, T;Nakano, N;Nishiyama, C
• 通讯作者: Nishiyama, C

Role of Sp1 in transcription of human ATP2A2 gene promoter in keratinocytes

Sp1 在角质形成细胞中人 ATP2A2 基因启动子转录中的作用

• 发表时间: 2008
• 期刊: J. Invest. Dermatol 128
• 作者: Takagi;A.;Nishiyama;C.;Maeda;K.;Tokura;T.;Kawada;H.;Kanada;S.;Niwa;Y.;Nakano;N.;Mayuzumi;N.;Nishiyama;M.;Ikeda;S.;Okumura;K.;Ogawa;H.
• 通讯作者: H.

皮膚疾患の最新医療、「アトピー性皮膚炎の疾患感受性遺伝子」

皮肤病最新医学疗法：“特应性皮炎的疾病易感基因”

• 发表时间: 2006
• 作者: Inoue M;Takahashi K;Niide O;Shibata M;Fukuzawa M;Ra C;KURATA Nobuo;西村秀雄;松尾弘;西山 千春
• 通讯作者: 西山 千春