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NICKβ2-糖蛋白I(B2GPI)通过其结构域V与血管抑素结合并发挥促血管生成作用(Nakagawa等人)。血液2009)。本研究的目的是探讨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得到表达。用抗FLAG柱或镍柱对产物进行纯化。用表面等离子共振技术检测完整/缺失的b2GPI结构域V与血管抑素4.5(AS4.5)的结合。缺失的b2GPI结构域V在Kd为5×10-8M时与AS4.5特异性结合,而完整的b2GPI结构域V无特异性结合。人脐静脉内皮细胞(HUVECs)在存在或不存在完整/有缺口b2GPI结构域V的情况下进行细胞增殖实验,完整和有缺口的b2GPI结构域V在0.4uM时对细胞的增殖有轻微的抑制作用。
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
Diagnosis and treatment of RA in Japan
日本RA的诊断和治疗
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[Matsumoto, M., Nishikawa, Y., Mouri, Y., Hirota, F., Nishijima, H, Yasuda S]
通讯作者:
Yasuda S
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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]
通讯作者:
Yasuda S
Essential role of the p38 mitogen-activated protein kinase pathway in tissue factor gene expression mediated by the phosphatidylserine-dependent antiprothrombin antibody.
p38 丝裂原激活蛋白激酶途径在磷脂酰丝氨酸依赖性抗凝血酶原抗体介导的组织因子基因表达中的重要作用。
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:
Atsumi T.
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