Liu Yuqing, Guan Lizhao, Zhan Jun, Lu Danyu, Wan Junhu, Zhang Hongquan
Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Peking University Health Science Center, Beijing 100191, China; State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing 100191, China; Laboratory of Molecular Cell Biology and Tumor Biology, Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing 100191, China.
Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Peking University Health Science Center, Beijing 100191, China; State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing 100191, China; Laboratory of Molecular Cell Biology and Tumor Biology, Department of Anatomy, Histology and Embryology, Peking University Health Science Center, Beijing 100191, China.
FEBS Lett. 2014 Aug 25;588(17):2859-66. doi: 10.1016/j.febslet.2014.06.049. Epub 2014 Jul 2.
Unconventional myosin VIIA (Myo7a) has been known to associate with hereditary deafness. Here we present a novel function of Myo7a by identifying that Myo7a directly interacts with integrin β5 subunit and regulates cell adhesion and motility in an integrin-dependent manner. We found that Myo7a bound to the cytoplasmic tail of integrin β5. Further, we pinpointed an integrin-binding domain at F3 of the first FERM domain and F1 of the second FERM domain. Functionally, Myo7a-induced cell adhesion and migration were mediated by integrin αvβ5. These findings indicated that Myo7a interacts with integrin β5 and selectively promotes integrin αvβ5-mediated cell migration.
非传统肌球蛋白VIIA（Myo7a）已知与遗传性耳聋有关。在此，我们通过鉴定Myo7a直接与整合素β5亚基相互作用并以整合素依赖性方式调节细胞粘附和运动，揭示了Myo7a的一种新功能。我们发现Myo7a与整合素β5的胞质尾部结合。此外，我们在第一个FERM结构域的F3和第二个FERM结构域的F1处确定了一个整合素结合结构域。在功能上，Myo7a诱导的细胞粘附和迁移由整合素αvβ5介导。这些发现表明，Myo7a与整合素β5相互作用，并选择性地促进整合素αvβ5介导的细胞迁移。
