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细胞肿胀和缺血/缺氧对磷脂酶A2同工型的激活作用。

Activation of PLA2 isoforms by cell swelling and ischaemia/hypoxia.

作者信息

Lambert I H, Pedersen S F, Poulsen K A

机构信息

Institute for Molecular Biology and Physiology, The August Krogh Building, Universitetsparken, Copenhagen Ø, Denmark.

出版信息

Acta Physiol (Oxf). 2006 May-Jun;187(1-2):75-85. doi: 10.1111/j.1748-1716.2006.01557.x.

Abstract

Phospholipase A2 (PLA2) activity is increased in mammalian cells in response to numerous stimuli such as osmotic challenge, oxidative stress and exposure to allergens. The increased PLA2 activity is seen as an increased release of free, polyunsaturated fatty acids, e.g. arachidonic acid and membrane-bound lysophospholipids. Even though arachidonic acid acts as a second messenger in its own most mammalian cells seem to rely on oxidation of the fatty acid into highly potent second messengers via, e.g. cytochrome P450, the cyclo-oxygenase, or the lipoxygenase systems for downstream signalling. Here, we review data that illustrates that stress-induced PLA2 activity involves various PLA2 subtypes and that the PLA2 in question is determined by the cell type and the physiological stress condition.

摘要

磷脂酶A2(PLA2)活性在哺乳动物细胞中会因多种刺激而增加,如渗透压挑战、氧化应激和接触过敏原。PLA2活性增加表现为游离多不饱和脂肪酸(如花生四烯酸)和膜结合溶血磷脂的释放增加。尽管花生四烯酸在大多数哺乳动物细胞中本身作为第二信使起作用,但细胞似乎依赖于通过细胞色素P450、环氧化酶或脂氧合酶系统等将脂肪酸氧化为高效的第二信使来进行下游信号传导。在此,我们综述了相关数据,这些数据表明应激诱导的PLA2活性涉及多种PLA2亚型,且所涉及的PLA2由细胞类型和生理应激条件决定。

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