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瞬时受体电位钙通道与视网膜变性。

The TRP calcium channel and retinal degeneration.

作者信息

Minke Baruch

机构信息

Department of Physiology and the Kühne Minerva Center for Studies of Visual Transduction, The Hebrew University-Hadassah Medical School Jerusalem 91120, Israel.

出版信息

Adv Exp Med Biol. 2002;514:601-22. doi: 10.1007/978-1-4615-0121-3_34.

Abstract

The Drosophila light activated channel TRP is the founding member of a large and diverse family of channel proteins that is conserved throughout evolution. These channels are Ca2+ permeable and have been implicated as important component of cellular Ca2+ homeostasis in neuronal and non-neuronal cells. The power of the molecular genetics of Drosophila has yielded several mutants in which constitutive activity of TRP leads to a rapid retinal degeneration in the dark. Metabolic stress activates rapidly and reversibly the TRP channels in the dark in a constitutive manner by a still unknown mechanism. The link of TRP gating to the metabolic state of the cell is shared also by mammalian homologues of TRP and makes cells expressing TRP extremely vulnerable to metabolic stress, a mechanism that may underlie retinal degeneration and neuronal cell death.

摘要

果蝇光激活通道TRP是一个庞大且多样的通道蛋白家族的创始成员,该家族在整个进化过程中都保守存在。这些通道对Ca2+具有通透性,并被认为是神经元和非神经元细胞中细胞Ca2+稳态的重要组成部分。果蝇分子遗传学的强大作用产生了几个突变体,其中TRP的组成型活性会导致在黑暗中视网膜迅速退化。代谢应激通过一种仍未知的机制,以组成型方式在黑暗中快速且可逆地激活TRP通道。TRP门控与细胞代谢状态的联系在TRP的哺乳动物同源物中也存在,这使得表达TRP的细胞极易受到代谢应激的影响,这种机制可能是视网膜退化和神经元细胞死亡的基础。

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