Vigh Laszlo, Nakamoto Hitoshi, Landry Jacques, Gomez-Munoz Antonio, Harwood John L, Horvath Ibolya
Institute of Biochemistry, Biology Research Centre, Hungarian Academy of Sciences,Temesvari krt 62, H-6726, Szeged, Hungary.
Ann N Y Acad Sci. 2007 Oct;1113:40-51. doi: 10.1196/annals.1391.027. Epub 2007 Jul 26.
"Membrane regulation" of stress responses in various systems is widely studied. In poikilotherms, membrane rigidification could be the first reaction to cold perception: reducing membrane fluidity of membranes at physiological temperatures is coupled with enhanced cold inducibility of a number of genes, including desaturases (see J.L. Harwood's article in this Proceedings volume). A similar role of changes in membrane physical state in heat (oxidative stress, etc.) sensing- and signaling gained support recently from prokaryotes to mammalian cells. Stress-induced remodeling of membrane lipids could influence generation, transduction, and deactivation of stress signals, either through global effects on the fluidity of the membrane matrix, or by specific interactions of boundary (or raft) lipids with receptor proteins, lipases, ion channels, etc. Our data point to membranes not only as targets of stress, but also as sensors in activating a stress response.
各种系统中应激反应的“膜调节”已得到广泛研究。在变温动物中,膜硬化可能是对冷感知的第一反应:在生理温度下降低膜的流动性与许多基因(包括去饱和酶)的冷诱导性增强相关(见本论文集里J.L. 哈伍德的文章)。最近,从原核生物到哺乳动物细胞,膜物理状态变化在热(氧化应激等)传感和信号传导中发挥的类似作用得到了支持。应激诱导的膜脂重塑可能通过对膜基质流动性的整体影响,或通过边界(或筏)脂与受体蛋白、脂肪酶、离子通道等的特异性相互作用,来影响应激信号的产生、转导和失活。我们的数据表明,膜不仅是应激的靶点,也是激活应激反应的传感器。