Generation and characterization of a functional Nanobody against the vascular endothelial growth factor receptor-2; angiogenesis cell receptor

被引：92

作者：

Behdani, Mandi

Zeinali, Sirous ^{[1
]}

Khanahmad, Hossein

Karimipour, Morteza

Asadzadeh, Nader

Azadmanesh, Keyhan ^{[2
]}

Khabiri, Alireza

Schoonooghe, Steve ^{[3
,4
]}

Anbouhi, Mahdi Habibi

Hassanzadeh-Ghassabeh, Gholamreza ^{[3
,4
]}

Muyldermans, Serge ^{[3
,4
]}

机构：

[1] Pasteur Inst Iran, Dept Mol Med, Biotechnol Res Ctr, Tehran 1316543551, Iran

[2] Pasteur Inst Iran, Dept Virol, Tehran 1316543551, Iran

[3] Vrije Univ Brussel, Cellular & Mol Immunol Lab, Brussels, Belgium

[4] VIB, NSF, Dept Biol Struct, Brussels, Belgium

来源：

MOLECULAR IMMUNOLOGY | 2012年 / 50卷 / 1-2期

关键词：

VEGFR2; Nanobody; Angiogenesis; SINGLE-DOMAIN ANTIBODIES; RAMUCIRUMAB IMC-1121B; INHIBITION; EXPRESSION; FRAGMENTS; SELECTION; IMMUNOGLOBULIN; AFFINITY; THERAPY; VEGFR-2;

D O I：

10.1016/j.molimm.2011.11.013

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Vascular endothelial growth factor receptor-2 (VEGFR2) is an important tumor-associated receptor and blockade of the VEGF receptor signaling can lead to the inhibition of neovascularization and tumor metastasis. Nanobodies are the smallest intact antigen binding fragments derived from heavy chain-only antibodies occurring in camelids. Here, we describe the identification of a VEGFR2-specific Nanobody, named 3VGR19, from dromedaries immunized with a cell line expressing high levels of VEGFR2. We demonstrate by FACS, that 3VGR19 Nanobody specifically binds VEGFR2 on the surface of 293KDR and HUVECs cells. Furthermore, the 3VGR19 Nanobody potently inhibits formation of capillary-like structures. These data show the potential of Nanobodies for the blockade of VEGFR2 signaling and provide a basis for the development of novel cancer therapeutics. (c) 2011 Elsevier Ltd. All rights reserved.

引用

页码：35 / 41

页数：7

共 47 条

[1] Cell selection and characterization of a novel human endothelial cell specific nanobody [J].