A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis
A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis
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DOI：
10.1016/s1074-7613(01)00232-1
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发表时间：
2001-11-01
期刊：
影响因子：
32.4
通讯作者：
Fanslow, WC
中科院分区：
文献类型：
--
作者：
Wiley, SR;Cassiano, L;Fanslow, WC
TWEAK 是 TNF 配体家族的成员，可诱导体内血管生成。我们报告从人脐静脉内皮细胞 (HUVEC) 库中克隆 TWEAK 受体 (TweakR)。 TweakR 的成熟形式在其胞外区仅含有 102 个氨基酸和 6 个半胱氨酸残基。五种不同的测定法证明了 TWEAK-TweakR 结合，并且相互作用亲和力常数 (Kd) 在 2.3 +/- 0.1 nM 的生理相关范围内。 TweakR 胞质结构域结合 TRAF 1、2 和 3。TweakR 的交联会诱导 HUVEC 生长，并且 mRNA 水平在体外通过多种药物上调，在体内动脉损伤后上调。可溶性 TweakR 抑制体外内皮细胞迁移和体内角膜血管生成。
TWEAK is a member of the TNF ligand family that induces angiogenesis in vivo. We report cloning of a receptor for TWEAK (TweakR) from a human umbilical vein endothelial cell (HUVEC) library. The mature form of TweakR has only one hundred and two amino acids and six cysteine residues in its extracellular region. Five different assays demonstrate TWEAK-TweakR binding, and the interaction affinity constant (Kd) is within a physiologically relevant range of 2.3 +/- 0.1 nM. The TweakR cytoplasmic domain binds TRAFs 1, 2, and 3. Cross-linking of TweakR induces HUVEC growth, and mRNA levels are upregulated in vitro by a variety of agents and in vivo following arterial injury. Soluble TweakR inhibits endothelial cell migration in vitro and corneal angiogenesis in vivo.