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首页> 外文期刊>Cellular Signalling >The absence of expression of the three isoenzymes of the inositol 1,4,5-trisphosphate 3-kinase does not prevent the formation of inositol pentakisphosphate and hexakisphosphate in mouse embryonic fibroblasts
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The absence of expression of the three isoenzymes of the inositol 1,4,5-trisphosphate 3-kinase does not prevent the formation of inositol pentakisphosphate and hexakisphosphate in mouse embryonic fibroblasts

机译：肌醇1,4,5-三磷酸3激酶的三种同工酶的缺乏表达不能阻止小鼠胚胎成纤维细胞中肌醇五磷酸和六磷酸的形成

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The activation of phospholipase C leads to the formation of both I(1,4,5)P-3 and diacylglycerol (DAG). I(1,4,5)P-3 can be metabolized by dephosphorylation catalyzed by Type II(1,4,5)P-3 5-phosphatase and by enzymatic phosphorylation to various inositol phosphates. This last step is catalyzed by three mammalian isoenzymes that specifically phosphorylate the 3-phosphate position of the inositol ring Itpka, Itpkb and Itpkc and a less specific enzyme Ipmk (or inositol multikinase) that phosphorylates I(1,4,5)P-3 at the D-3 and D-6 positions. This study was performed in mice cells in order to understand the synthetic pathway of IP5 and IP6 following PLC stimulation and possible link with Itpk activity. Mouse embryonic fibroblasts (MEF) were prepared from Itpkb(-/-) Itpkc(-/-) mice. Western blot and RT-PCR analysis show that the cells do not express Itpka. In contrast, they do express Ipmk. The cells still produce IP5 and IP6. Our data show that the absence of expression of the three isoenzymes of ItPk does not prevent the formation of IP5 and IP6, at least in mouse embryonic fibroblasts. The nuclear Ipmk plays therefore a critical role in the metabolism of 1(1,4,5)P-3 and production of highly phosphorylated IP5 and IP6. (c) 2007 Elsevier Inc. All rights reserved.
机译：磷脂酶C的激活导致I（1,4,5）P-3和二酰基甘油（DAG）的形成。 I（1,4,5）P-3可以通过II（1,4,5）P-3型5磷酸酶催化的去磷酸化和酶磷酸化为各种肌醇磷酸来代谢。这最后一步是由三种哺乳动物同工酶催化的，它们特异性磷酸化了肌醇环Itpka，Itpkb和Itpkc的3-磷酸位置，以及一种特异性较低的Impk酶（或肌醇多激酶），其磷酸化了I（1,4,5）P-3在D-3和D-6位置这项研究是在小鼠细胞中进行的，以了解PLC刺激后IP5和IP6的合成途径以及与Itpk活性的可能联系。从Itpkb（-/-）Itpkc（-/-）小鼠制备小鼠胚胎成纤维细胞（MEF）。蛋白质印迹和RT-PCR分析表明细胞不表达Itpka。相反，他们确实表达了Ipmk。单元仍然产生IP5和IP6。我们的数据表明，至少在小鼠胚胎成纤维细胞中，ItPk的三种同工酶的表达缺失不会阻止IP5和IP6的形成。因此，核Ipmk在1（1,4,5）P-3的代谢和高磷酸化IP5和IP6的产生中起关键作用。 （c）2007 Elsevier Inc.保留所有权利。

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