Wozniak Michele A, Modzelewska Katarzyna, Kwong Lina, Keely Patricia J
Department of Pharmacology, University of Wisconsin, 3630 MSC, 1300 University Ave, Madison 53706, USA.
Biochim Biophys Acta. 2004 Jul 5;1692(2-3):103-19. doi: 10.1016/j.bbamcr.2004.04.007.
Focal adhesions lie at the convergence of integrin adhesion, signaling and the actin cytoskeleton. Cells modify focal adhesions in response to changes in the molecular composition, two-dimensional (2D) vs. three-dimensional (3D) structure, and physical forces present in their extracellular matrix environment. We consider here how cells use focal adhesions to regulate signaling complexes and integrin function. Furthermore, we examine how this regulation controls complex cellular behaviors in response to matrices of diverse physical and biochemical properties. One event regulated by the physical structure of the ECM is phosphorylation of focal adhesion kinase (FAK) at Y397, which couples FAK to several signaling pathways that regulate cell proliferation, survival, migration, and invasion.
粘着斑位于整合素粘附、信号传导和肌动蛋白细胞骨架的交汇处。细胞会根据其细胞外基质环境中分子组成、二维(2D)与三维(3D)结构以及物理力的变化来改变粘着斑。我们在此探讨细胞如何利用粘着斑来调节信号复合物和整合素功能。此外,我们研究这种调节如何控制细胞对具有不同物理和生化特性的基质做出复杂的细胞行为反应。由细胞外基质的物理结构调节的一个事件是粘着斑激酶(FAK)在Y397位点的磷酸化,这将FAK与几个调节细胞增殖、存活、迁移和侵袭的信号通路联系起来。