Department of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Mol Cell. 2014 May 8;54(3):329-30. doi: 10.1016/j.molcel.2014.04.020.
In this issue of Molecular Cell, Wang et al. (2014) report that the splicing kinase SRPK1 can function as both an oncogene and a tumor suppressor by modulating the activation state of the protein kinase Akt. This is shown to be mediated by the ability of SRPK1 to bind to the Akt phosphatase PHLPP1.
在本期《分子细胞》中，Wang 等人（2014 年）报道称剪接激酶 SRPK1 可通过调节蛋白激酶 Akt 的激活状态，充当癌基因和抑癌基因。这是通过 SRPK1 与 Akt 磷酸酶 PHLPP1 结合的能力来介导的。
