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首页> 外文期刊>Advances in enzyme regulation >Inositides in the nucleus: further developments on phospholipase C beta 1 signalling during erythroid differentiation and IGF-I induced mitogenesis.
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Inositides in the nucleus: further developments on phospholipase C beta 1 signalling during erythroid differentiation and IGF-I induced mitogenesis.

机译：核中的肌苷：在红系分化和IGF-1诱导有丝分裂过程中磷脂酶C beta 1信号的进一步发展。

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摘要

Inositol lipids originally shown to be metabolized in the cytosol have been detected also in the nucleus, where they are both synthesized and hydrolyzed. In the case of erythroid differentiation of murine erythroleukemia cells (Friend cells) it has been previously shown that PLC beta 1, which is the major nuclear PLC, undergoes down-regulation upon treatment with DMSO or tiazofurin which act as differentiative agents. On the contrary, i.e., during IGF-I induced mitogenesis, it has been shown that PLC beta 1 is rapidly activated and this event is essential for the onset of DNA synthesis. Even though its key role in cell growth has been shown, both the mechanism by which nuclear PLC beta 1 is activated and the direct relationship with erythroid differentiation are still unknown. We have addressed the question if PLC beta 1 expression and activity in the nucleus are directly related or not to the establishment of the differentiated state and we have checked the two main ways of activation, i.e., via G-protein or via phosphorylation, in order to establish whether nuclear PLC beta 1 is regulated the same way as the one at the plasma membrane or not. The data reported here show that nuclear PLC beta 1 is responsible for a continuous recycling of Friend cells, acting as a negative regulator of differentiation and that its activation is dependent on the phosphorylation state.
机译：最初在细胞质中代谢的肌醇脂质也已经在细胞核中被检测到，在细胞核中它们都被合成并被水解。在鼠类红细胞白血病细胞（Friend细胞）的类红细胞分化的情况下，先前已显示，作为主要核PLC的PLC beta 1在用作为分化剂的DMSO或噻唑呋林处理后会下调。相反，即在IGF-1诱导的有丝分裂过程中，已经表明PLCβ1被迅速激活，并且该事件对于DNA合成的开始是必不可少的。尽管已表明其在细胞生长中的关键作用，但核PLC beta 1的激活机制以及与类红细胞分化的直接关系仍然未知。我们已经解决了PLC beta 1在细胞核中的表达和活性与分化状态的建立是否直接相关的问题，并且我们检查了两种主要激活方式，即通过G蛋白或通过磷酸化，依次确定核PLC beta 1的调控方式是否与质膜的调控方式相同。此处报道的数据表明，核PLC beta 1负责Friend细胞的连续回收，充当分化的负调节剂，其活化取决于磷酸化状态。

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