Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, Department of Cancer Biology, Madrid, Spain.
FEBS Lett. 2012 May 21;586(10):1533-9. doi: 10.1016/j.febslet.2012.04.017. Epub 2012 Apr 25.
We describe in this report the presence of a nuclear localization signal (NLS) overlapping the calmodulin-binding domain (CaM-BD) of the growth factor receptor bound protein 7 (Grb7). We show that deletion of the CaM-BD of Grb7 prevents its nuclear localization, and that its Src homology 2 (SH2) domain might participate as well in the translocation process. Also, treating cells with the CaM antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) enhances the presence of Grb7 in the nucleus. We propose that CaM inhibits the translocation of Grb7 to the nucleus after binding to its CaM-BD and therefore occluding its overlapping NLS.
我们在本报告中描述了生长因子受体结合蛋白 7（Grb7）的钙调蛋白结合域（CaM-BD）重叠的核定位信号（NLS）的存在。我们表明，Grb7 的 CaM-BD 缺失会阻止其核定位，其Src 同源 2（SH2）结构域也可能参与转位过程。此外，用钙调蛋白拮抗剂 N-（6-氨基己基）-5-氯-1-萘磺酰胺（W-7）处理细胞会增加 Grb7 在核内的存在。我们提出，钙调蛋白与 CaM-BD 结合后抑制 Grb7 向核内的转位，从而阻断其重叠的 NLS。
