核骨架的去聚化
中文名称
通路描述
有丝分裂前期核膜破裂涉及核骨架纤维的去聚化，核骨架的主要成分是核骨架纤维。核骨架位于内核膜的核面，在核膜的结构和功能中起重要作用（参见 Burke 和 Stewart 2012）。核骨架纤维的去聚化是由核骨架纤维的去聚化触发的，这些纤维由通过静电相互作用在头部到尾部分子链中相互结合的核骨架同源二聚体组成。CDK1 磷酸化核骨架的 N 端（Heald 和 McKeon 1990, Peter 等人 1990, Ward 和 Kirschner 1990, Mall 等人 2012），而 PKCs（PRKCA 和 PRKCB）磷酸化核骨架的 C 端（Hocevar 等人 1993, Goss 等人 1994, Mall 等人 2012）。PKCs 由脂质介导的信号激活，其中脂蛋白，由 CTDNEP1:CNEP1R1 丝氨酸/苏氨酸蛋白磷酸酶复合物激活，催化 DAG（Gorjanacz 等人 2009, Golden 等人 2009, Wu 等人 2011, Han 等人 2012, Mall 等人 2012）的形成。
英文描述
Depolymerization of the Nuclear Lamina The nuclear envelope breakdown in mitotic prophase involves depolymerization of lamin filaments, the main constituents of the nuclear lamina. The nuclear lamina is located at the nuclear face of the inner nuclear membrane and plays and important role in the structure and function of the nuclear envelope (reviewed by Burke and Stewart 2012). Depolymerization of lamin filaments, which consist of lamin homodimers associated through electrostatic interactions in head-to-tail molecular strings, is triggered by phosphorylation of lamins. While CDK1 phosphorylates the N-termini of lamins (Heald and McKeon 1990, Peter et al. 1990, Ward and Kirschner 1990, Mall et al. 2012), PKCs (PRKCA and PRKCB) phosphorylate the C-termini of lamins (Hocevar et al. 1993, Goss et al. 1994, Mall et al. 2012). PKCs are activated by lipid-mediated signaling, where lipins, activated by CTDNEP1:CNEP1R1 serine/threonine protein phosphatase complex, catalyze the formation of DAG (Gorjanacz et al. 2009, Golden et al. 2009, Wu et al. 2011, Han et al. 2012, Mall et al. 2012).
所含基因
15 个基因