Montell Denise J
Department of Biological Chemistry, Johns Hopkins University, Baltimore, MD 21205, USA.
Cell. 2006 Aug 11;126(3):450-2. doi: 10.1016/j.cell.2006.07.017.
Two new papers (Kuranaga et al., 2006; Oshima et al., 2006) describe a previously uncharacterized Drosophila kinase (DmIKK epsilon) that regulates the abundance of DIAP1, a protein best known for its ability to inhibit apoptosis. However, DmIKK epsilon-mediated degradation of DIAP1 does not regulate apoptosis as might be predicted but instead regulates actin dynamics, cell morphology, and the differentiation of sensory organ precursor cells.
两篇新论文（仓永等人，2006年；大岛等人，2006年）描述了一种以前未被鉴定的果蝇激酶（DmIKKε），它调节DIAP1的丰度，DIAP1是一种因其抑制细胞凋亡的能力而最为人所知的蛋白质。然而，DmIKKε介导的DIAP1降解并不像预期的那样调节细胞凋亡，而是调节肌动蛋白动力学、细胞形态以及感觉器官前体细胞的分化。
