Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6840, USA.
J Cell Physiol. 2010 Jun;223(3):541-8. doi: 10.1002/jcp.22107.
Laminin-332 (Ln-332) is an extracellular matrix molecule that regulates cell adhesion, spreading, and migration by interaction with cell surface receptors such as alpha3beta1 and alpha6beta4. Previously, we developed a function-blocking monoclonal antibody against rat Ln-332, CM6, which blocks hemidesmosome assembly induced by Ln-332-alpha6beta4 interactions. However, the location of its epitope on Ln-332 has remained unclear. In this study, we show that the CM6 epitope is located on the laminin G-like (LG)2 module of the Ln-332 alpha3 chain. To specify the residues involved in this epitope, we produced a series of GST-fused alpha3 LG2 mutant proteins in which rat-specific acids were replaced with human acids by a site-directed mutagenesis strategy. CM6 reactivity against these proteins showed that CM6 binds to the (1089)NERSVR(1094) sequence of rat Ln-332 LG2 module. In a structural model, this sequence maps to an LG2 loop sequence that is exposed to solvent according to predictions, consistent with its accessibility to antibody. CM6 inhibits integrin-dependent cell adhesion on Ln-332 and inhibits cell spreading on both Ln-332 and recombinant LG2 (rLG2; but not rLG3), suggesting the presence of an alpha3beta1 binding site on LG2. However, we were unable to show that rLG2 supports adhesion in standard assays, suggesting that LG2 may contain a "weak" integrin binding site, only detectable in spreading assays that do not require washes. These results, together with our previous findings, indicate that binding sites for alpha3beta1 and alpha6beta4 are closely spaced in the Ln-332 LG domains where they regulate alternative cell functions, namely adhesion/migration or hemidesmosome anchoring.
层粘连蛋白-332(Ln-332)是一种细胞外基质分子,通过与细胞表面受体(如α3β1 和α6β4)相互作用,调节细胞黏附、铺展和迁移。先前,我们开发了一种针对大鼠 Ln-332 的功能阻断单克隆抗体 CM6,它可以阻断 Ln-332-α6β4 相互作用诱导的半桥粒组装。然而,其在 Ln-332 上的表位位置仍不清楚。在这项研究中,我们表明 CM6 表位位于 Ln-332α3 链的层粘连蛋白 G 样(LG)2 模块上。为了确定该表位涉及的残基,我们通过定点突变策略用人类氨基酸取代大鼠特异性氨基酸,生成了一系列 GST 融合的α3LG2 突变蛋白。CM6 对这些蛋白的反应表明,CM6 结合大鼠 Ln-332 LG2 模块的(1089)NERSVR(1094)序列。在结构模型中,该序列映射到 LG2 环序列,根据预测,该序列暴露在溶剂中,与抗体的可及性一致。CM6 抑制整合素依赖的细胞在 Ln-332 上的黏附,并抑制细胞在 Ln-332 和重组 LG2(rLG2;但不包括 rLG3)上的铺展,表明 LG2 上存在一个α3β1 结合位点。然而,我们无法证明 rLG2 在标准测定中支持黏附,这表明 LG2 可能包含一个“弱”整合素结合位点,仅在不需要洗涤的铺展测定中才能检测到。这些结果与我们之前的发现一起表明,α3β1 和α6β4 的结合位点在 Ln-332 LG 结构域中紧密排列,在这些结构域中,它们调节替代的细胞功能,即黏附/迁移或半桥粒锚定。