Role of recombinant nicked beta2-glycoprotein I domain V in angiogenesis
Role of recombinant nicked beta2-glycoprotein I domain V in angiogenesis
批准号:
23591431
负责人:
YASUDA Shinsuke
金额:
$3.24万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2011
资助国家:
日本
项目状态:
已结题
起止时间:
2011 至 2013
中文摘要
先前我们报道了缺口β -糖蛋白I (b2GPI)通过其结构域V与血管抑制素结合并发挥促血管生成作用(Nakagawa等)。血2009)。本研究旨在探讨b2GPI结构域V在血管生成中的作用。重组b2GPI结构域V在哺乳动物细胞表达系统和细菌中生成。采用反flag柱或镍柱对产物进行纯化。利用表面等离子体共振评估完整/缺口b2GPI结构域V与血管抑制素4.5 (AS4.5)之间的结合。缺失的b2GPI结构域V在KD为~ 5 × 10-8M时特异性结合到AS4.5上,而完整的b2GPI结构域V没有特异性结合。使用人脐带内皮细胞(HUVECs)进行细胞增殖实验,在存在或不存在完整的/缺口的b2GPI结构域V的情况下,完整的和缺口的b2GPI结构域V在0.4uM时均能轻微抑制细胞增殖。综上所述,b2GPI的切口结构域V与AS4.5结合,在整个b2GPI中观察到切口形式。
英文摘要
Previously we reported nicked beta2-glycoprotein I (b2GPI) binds to angiostatin via its domain V and exerts pro-angiogenic effect (Nakagawa et al. Blood 2009). The aim of this study was to investigate the role of b2GPI domain V in angiogenesis. Recombinant b2GPI domain V was generated in mammalian cell expression system and bacteria. Purification of the product was done using anti-FLAG column or nickel column. Binding between intact/nicked b2GPI domain V and angiostatin 4.5 (AS4.5) was evaluated using surface plasmon resonance. Nicked b2GPI domain V specifically bound onto AS4.5 at KD of ~ 5 x 10-8M, whereas intact b2GPI domain V showed no specific binding. Cell proliferation assay using human umbilical endothelial cells (HUVECs) were performed in the presence or absence of intact/nicked b2GPI domain V. Both intact and nicked b2GPI domain V slightly inhibited cell proliferation at 0.4uM.In conclusion, nicked b2GPI domain V bound to AS4.5, as observed in nicked form of whole b2GPI.
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The involvement of CD36 in monocyte activation by antiphospholipid antibodies.
CD36 参与抗磷脂抗体激活单核细胞。
DOI:
10.1177/0961203313490242
发表时间:
2013
期刊:
Lupus
影响因子:
2.6
作者:
[Kato M, Atsumi T, Oku K, Amengual O, Nakagawa H, Fujieda Y, Otomo K, Horita T, Yasuda S, Koike T.]
通讯作者:
Koike T.
Role of β2-glycoprotein I Domain V in Angiogenesis
β2-糖蛋白 I 结构域 V 在血管生成中的作用
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[Yasuda S, Kubota A, Nakagawa H, Kuroki K, Fujieda Y, Bohgaki T, Amengual O, Horita T, Maenaka K, Atsumi T]
通讯作者:
Atsumi T
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日本RA的诊断和治疗
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
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通讯作者:
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抗磷脂抗体存在下的弥散性血管内凝血:与灾难性或微血管病性抗磷脂综合征的鉴别诊断
DOI:
--
发表时间:
2013
期刊:
Intern Med
影响因子:
--
作者:
[細野治, 上原昌晃, 松宮遼, 吉川賢忠, 小林浩, 鈴木幸男, 田中廣壽, Yasuda S]
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Yasuda S
Essential role of the p38 mitogen-activated protein kinase pathway in tissue factor gene expression mediated by the phosphatidylserine-dependent antiprothrombin antibody.
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DOI:
10.1093/rheumatology/ket234
发表时间:
2013
期刊:
Rheumatology (Oxford).
影响因子:
--
作者:
[Oku K, Amengual O, Zigon P, Horita T, Yasuda S, Atsumi T.]
通讯作者:
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共 38 条
Abnormal expressions of RasGRPs in autoimmune diseases
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批准号:20591163
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.83万
-
财政年份:2008
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负责人:YASUDA Shinsuke
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依托单位:
海外基金