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首页> 外文期刊>Advances in enzyme regulation >Signal transduction within the nucleus: Revisiting phosphoinositide inositide-specific phospholipase Cbetai
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Signal transduction within the nucleus: Revisiting phosphoinositide inositide-specific phospholipase Cbetai

机译：核内信号转导：重新审视磷酸肌醇，肌苷特异性磷脂酶Cbetai

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摘要

In the nucleus the existence of both polyphosphoinositides and the enzymes responsible for their metabolism clearly indicates that they may constitute an autonomous lipid-dependent signaling system (Irvine, 2003; Manzoli et al., 2005). Indeed nuclear inositol lipid metabolism is independently regulated from its plasma membrane counterpart and is modulated in response to short-term growth factor stimulation, cell cycle progression and during differentiation (Martelli et al., 2004). Phosphoinositide-specific phospholipase C (PI-PLC) is a key player in the regulation of nuclear inositol lipid signaling. PI-PLC catalyzes phosphatidylinositol (4,5)-bisphosphate (PtdIns(4,5)P_2) hydrolysis to yield two fundamental second messengers: inositol (l,4,5)-trisphosphate (Ins(l,4,5)P_3) and diacyl-glycerol (DG). Several PI-PLC isoforms have been identified in the nucleus but the -fii isozyme is the best characterized (Cocco et al., 2001). In response to short term stimulation of quiescent Swiss 3T3 cells with IGF-1,nuclear PI-PLCbeta_1 is activated by p42/44 MAPK-dependent phosphorylation and subsequently down-regulated by another phosphorylation step effected by protein kinase C-alpha (PKC-a), which is attracted to the nucleus by the DG produced by PI-PLCbeta_1 (Xu et al., 2001a, b). Overexpression of PI-PLCbeta_1 in the nucleus is sufficient to drive 3T3 cells into S phase (Xu et al., 2001a).
机译：在细胞核中，多磷酸肌醇和负责其代谢的酶的存在清楚地表明它们可能构成了自主的脂质依赖性信号传导系统（Irvine，2003; Manzoli等，2005）。实际上，核肌醇脂质代谢与其质膜对应物是独立调节的，并且响应于短期生长因子刺激，细胞周期进程以及分化过程而被调节（Martelli等，2004）。磷脂酰肌醇特异性磷脂酶C（PI-PLC）是调节核肌醇脂质信号传导的关键参与者。 PI-PLC催化磷脂酰肌醇（4,5）-双磷酸（PtdIns（4,5）P_2）水解产生两个基本的第二信使：肌醇（1,4,5）-三磷酸（Ins（1,4,5）P_3）和二酰基甘油（DG）。在细胞核中已鉴定出几种PI-PLC同工型，但-fii同工酶的特征最为明显（Cocco等，2001）。为响应使用IGF-1对静止的Swiss 3T3细胞的短期刺激，核PI-PLCbeta_1被p42 / 44 MAPK依赖性磷酸化激活，随后被蛋白激酶C-α（PKC-a）影响的另一个磷酸化步骤下调），它被PI-PLCbeta_1产生的DG吸引到细胞核上（Xu等，2001a，b）。 PI-PLCbeta_1在细胞核中的过表达足以驱动3T3细胞进入S期（Xu等，2001a）。

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