The Mechanisms Involved in Chemotaxis of Immune and Cancer Cells

我们有两个项目。 1. CXCR 4受体如何通过信号传导至埃尔莫/Dock复合物从而形成肌动蛋白细胞骨架？ 我们在D. discoideum揭示了一种新的途径，将G蛋白亚基直接连接到埃尔莫/Dock复合物。 我们正在研究这在人类趋化因子受体控制的细胞迁移中是否是进化保守的。2. β-arrestin在中性粒细胞趋化性中的作用。 已知活化的趋化因子GPCR与β-抑制蛋白相互作用，β-抑制蛋白带来信号传导组分并激活不依赖于G蛋白的通路。 已经表明β-抑制蛋白信号传导在细胞迁移中起作用，但这一过程的分子机制尚不清楚。 我们正在利用中性粒细胞研究这些机制。

We have two projects. 1. How does CXCR4 receptor signaling to Elmo/Dock complex leading to actin cytoskeleton? Our study in D. discoideum revealed a novel pathway linking G-protein subunits directly to Elmo/Dock complex. We are in the process to investigate whether this is evolutionarily conserved in chemokine receptor-controlled cell migration in human. 2. The role of beta-arrestin in neutrophil chemotaxis. It is known that activated chemokine GPCRs interact with beta-arrestin, which brings signaling components and activates pathways independent of G-proteins. It has been suggested that beta-arrestin signaling plays a role in cell migration, but the molecular mechanisms underlining this process are not known. We are in the process to study these mechanisms using neutrophils.