Analysis of CD26 mediated signal transduction mechanism.

CD26介导的信号转导机制分析。

基本信息

  • 批准号:
    09044266
  • 负责人:
  • 金额:
    $ 2.56万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for international Scientific Research
  • 财政年份:
    1997
  • 资助国家:
    日本
  • 起止时间:
    1997 至 1998
  • 项目状态:
    已结题

项目摘要

CD26, a 110 kDa cell surface glycoprotein, exhibits dipeptidyl peptidase IV (DPPIV ; EC3.4.14.5) enzyme activity and plays an important role in T cell costimulation. the function of CD26/dipeptidyl peptidase IV in transendothelial migration was examined using beta-chemokines as chemoattractants. When soluble recombinant CD26 (sCD26/DPPIV^+) was added to the transendothelial chemotaxis system, chemotactic migration of T cells toward RANTES was significantly enhanced. Addition of sCD26 to 50 ng/ml of RANTES enhanced the migratory response by a factor of two compared to RANTES alone, whereas mutant soluble CD26, lacking the DPPIV enzyme activity, had no enhancing effect on RANTES-induced T cell migration. In the process of analyzing the mechanisms of the enhancement of T cell migration by sCD26, we showed that RANTES was cleaved by sCD26 under physiologic conditions at the precise site characteristic of its enzyme specificity. However, synthesized RANTES which lacks two N-terminal amino a … More cids showed a chemotactic activity equivalent to full length RANTES on T cells. Furthermore, addition of sCD26 showed enhancement of T cell migration induced by both forms of RANTES.In contrast to T cells, the truncated RANTES is inactive in chemotaxis of purified monocytes, and supplement of sCD26 but not mCD26 reduced the migratory response of monocytes to RANTES.These results suggest that CD26/DPPIV differentially regulate the chemotactic response of T cells and monocytes to RANTES and furthermore, the finding can partly explain the dominant phenotype at the chronic inflammatory sites in vivo. Stromal cell-derived factor 1alpha (SDF-1alpha) is a chemokine that has been shown to prevent infection of T-tropic HIV strains and is a possible substrate of CD26/DPPIV.We have shown that SDF-1alpha was cleaved at the N-terminal region by CD26/DPPIV and as a result, the inhibitory activity of SDF-1alpha against HIV infection was disappeared. Moreover, the chemotactic activity of SDF-1alpha was also disappeared specifically by DPPIV activity of recombinant soluble CD26. These results suggested that dissemination of T-tropic HIV strains in vivo may be facilitated by CD26/DPPIV via inactivation of functional SDF-1alpha. Less
CD 26是一种110 kDa的细胞表面糖蛋白,具有二肽基肽酶IV(DPPIV ; EC3.4.14.5)酶活性,在T细胞共刺激中起重要作用。使用β-趋化因子作为化学引诱物检测了CD 26/二肽基肽酶IV在跨内皮迁移中的功能。当可溶性重组CD 26(sCD 26/DPPIV^+)加入到跨内皮趋化系统中时,T细胞向RANTES的趋化迁移显著增强。添加sCD 26到50 ng/ml的RANTES增强迁移反应的一个因素的两个单独的RANTES相比,而突变的可溶性CD 26,缺乏DPPIV酶的活性,没有增强作用RANTES诱导的T细胞迁移。在分析sCD 26增强T细胞迁移的机制的过程中,我们发现RANTES在生理条件下在其酶特异性的精确位点被sCD 26切割。然而,合成的RANTES缺乏两个N-末端氨基, ...更多信息 cids对T细胞显示出与全长RANTES相当的趋化活性。此外,添加sCD 26可增强两种形式RANTES诱导的T细胞迁移。与T细胞相反,截短的RANTES对纯化单核细胞的趋化性无活性,并且添加sCD 26(而不是mCD 26)可降低单核细胞对RANTES的迁移反应。这些结果表明CD 26/DPPIV差异调节T细胞和单核细胞对RANTES的趋化反应,此外,这一发现可以部分解释体内慢性炎症部位的优势表型。基质细胞衍生因子1 α(SDF-1 α)是一种趋化因子,已被证明可以防止T嗜性HIV株的感染,并且是CD 26/DPPIV的可能底物。我们已经证明,SDF-1 α在N-末端区域被CD 26/DPPIV切割,因此,SDF-1 α对HIV感染的抑制活性消失。此外,SDF-1 α的趋化活性也被重组可溶性CD 26的DPPIV活性特异性地消除。这些结果表明,T嗜性HIV株在体内的传播可能是通过CD 26/DPPIV通过功能性SDF-1 α的失活而促进的。少

项目成果

期刊论文数量(22)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Ohtsuki T: "Negative regulation of the anti‐HIV and chemotactic activity of human stromal cell-derived factor 1α by CD26/DPPIV." FEBS Letter. 431. 236-240 (1998)
Ohtsuki T:“CD26/DPPIV 对人基质细胞衍生因子 1α 的抗 HIV 和趋化活性的负调节。”FEBS Letter。431. 236-240 (1998)
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Hegen M: "Cross-linking of CD26 by antibody induces tyrosine phosphorylation and activation of mitogen-activated protein kinase." Immunol.90. 257-264 (1997)
Hegen M:“抗体交联 CD26 会诱导酪氨酸磷酸化和丝裂原激活蛋白激酶的激活。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Hegen M,Kameoka J,Dong RP,Schlossman SF,and Morimoto C.: "Cross-linking of CD26 by antibody induces tyrosine phosphorylation and activation of mitogen-activated protein kinase." Immunol.90. 257-264 (1997)
Hegen M、Kameoka J、Dong RP、Schlossman SF 和 Morimoto C.:“抗体交联 CD26 会诱导酪氨酸磷酸化和丝裂原激活蛋白激酶的激活。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Dong R-P,Tachibana K,Hegen M,Soherpe S,Cho D,Schlossman SF,and Morimoto C.: "Correlation of the epitope defined by anti-CD26 mAbs and CD26 function." Mol.Immunol.35. 13-21 (1998)
Dong R-P、Tachibana K、Hegen M、Soherpe S、Cho D、Schlossman SF 和 Morimoto C.:“抗 CD26 mAb 定义的表位与 CD26 功能的相关性。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Dong R-P,Umezawa Y,Ikushima H,Munakata Y,Schlossman SF,and Morimoto C.: "Different regulatory effects of pentoxifylline on human T cell activation pathways." J.Clin.Immunol.17. 247-252 (1997)
Dong R-P、Umezawa Y、Ikushima H、Munakata Y、Schlossman SF 和 Morimoto C.:“己酮可可碱对人类 T 细胞激活途径的不同调节作用。”
  • DOI:
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  • 期刊:
  • 影响因子:
    0
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MORIMOTO Chikao其他文献

MORIMOTO Chikao的其他文献

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{{ truncateString('MORIMOTO Chikao', 18)}}的其他基金

Association of deubiquitin ligase and cell surface molecules regulates the pathophysiology of malignant pleural mesothelioma
去泛素连接酶和细胞表面分子的关联调节恶性胸膜间皮瘤的病理生理学
  • 批准号:
    24659401
  • 财政年份:
    2012
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
To determine the epigenetic regulatory mechanism of cancer stem cells by cell surface molecules.
通过细胞表面分子确定癌症干细胞的表观遗传调控机制。
  • 批准号:
    22650223
  • 财政年份:
    2010
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Basic research of defining the function of CD26 on human immune system and its clinical application for autoimmune diseases.
CD26对人体免疫系统功能的基础研究及其在自身免疫性疾病中的临床应用。
  • 批准号:
    22390200
  • 财政年份:
    2010
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Basic Approach for the Development of Molecular Target Therapy for Autoimmune Diseases and Immune-Mediated Disorders.
开发自身免疫性疾病和免疫介导疾病分子靶向治疗的基本方法。
  • 批准号:
    17109011
  • 财政年份:
    2005
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Scientific Research (S)
Basic study of molecular target therapy for autoimmune diseases and immune deficiency diseases based on CD26
基于CD26的自身免疫性疾病及免疫缺陷病分子靶向治疗基础研究
  • 批准号:
    15209033
  • 财政年份:
    2003
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
The development of specific immune regulatory drugs utilizing the structure and function of CD26
利用CD26的结构和功能开发特异性免疫调节药物
  • 批准号:
    13557039
  • 财政年份:
    2001
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analysis of the function of lymphocyte adhesion molecules and its clinical significances in autoimmune diseases
淋巴细胞粘附分子在自身免疫性疾病中的功能分析及其临床意义
  • 批准号:
    13470107
  • 财政年份:
    2001
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analysis of CD29/VLA integrin in T cell immune regulation and its clinical significance
CD29/VLA整合素在T细胞免疫调节中的作用分析及其临床意义
  • 批准号:
    11307009
  • 财政年份:
    1999
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A).
Structure and function of memory T cell marker CD26
记忆T细胞标志物CD26的结构和功能
  • 批准号:
    11694248
  • 财政年份:
    1999
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B).
Development of specific imuune regulatoly drugs by the cell surface molecules.
利用细胞表面分子开发特异性免疫调节药物。
  • 批准号:
    10557049
  • 财政年份:
    1998
  • 资助金额:
    $ 2.56万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)

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Active involvements of glucagon-like peptide-1 (GLP-1) / dipeptidyl peptidase IV (DPP4) system in the development of renal injury in a rat model of chronic kidney disease (CKD).
胰高血糖素样肽-1 (GLP-1)/二肽基肽酶 IV (DPP4) 系统积极参与慢性肾病 (CKD) 大鼠模型肾损伤的发生。
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二肽基肽酶-IV 在先天免疫反应中的作用
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    nhmrc : 1016662
  • 财政年份:
    2011
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    8168062
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    2010
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  • 财政年份:
    2009
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眼镜王蛇二肽基肽酶 IV 的结构/药理学
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    7667994
  • 财政年份:
    2008
  • 资助金额:
    $ 2.56万
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Therapeutic potential of the dipeptidyl peptidase IV gene family
二肽基肽酶 IV 基因家族的治疗潜力
  • 批准号:
    nhmrc : 512282
  • 财政年份:
    2008
  • 资助金额:
    $ 2.56万
  • 项目类别:
    NHMRC Project Grants
P4-ROLE OF DIPEPTIDYL PEPTIDASE IV IN PERIPHERAL NEUROGENESIS AND NEUROBLASTOMAS
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    7725303
  • 财政年份:
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    7609873
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    2007
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Neuropeptide Y and dipeptidyl-peptidase IV (CD26) in chronic fatigue syndrome
神经肽 Y 和二肽基肽酶 IV (CD26) 在慢性疲劳综合征中的作用
  • 批准号:
    7126969
  • 财政年份:
    2006
  • 资助金额:
    $ 2.56万
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Neuropeptide Y and dipeptidyl-peptidase IV (CD26) in chronic fatigue syndrome
神经肽 Y 和二肽基肽酶 IV (CD26) 在慢性疲劳综合征中的作用
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    7296144
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