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在缺乏极低密度脂蛋白受体和载脂蛋白E受体2的基因敲除小鼠中,Reeler/Disabled样神经元迁移紊乱。

Reeler/Disabled-like disruption of neuronal migration in knockout mice lacking the VLDL receptor and ApoE receptor 2.

作者信息

Trommsdorff M, Gotthardt M, Hiesberger T, Shelton J, Stockinger W, Nimpf J, Hammer R E, Richardson J A, Herz J

机构信息

Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235-9046, USA.

出版信息

Cell. 1999 Jun 11;97(6):689-701. doi: 10.1016/s0092-8674(00)80782-5.

Abstract

Layering of neurons in the cerebral cortex and cerebellum requires Reelin, an extracellular matrix protein, and mammalian Disabled (mDab1), a cytosolic protein that activates tyrosine kinases. Here, we report the requirement for two other proteins, cell surface receptors termed very low density lipoprotein receptor (VLDLR) and apolipoprotein E receptor 2 (ApoER2). Both receptors can bind mDab1 on their cytoplasmic tails and are expressed in cortical and cerebellar layers adjacent to layers that express Reelin. mDab1 expression is upregulated in knockout mice that lack both VLDLR and ApoER2. Inversion of cortical layers and absence of cerebellar foliation in these animals precisely mimic the phenotype of mice lacking Reelin or mDab1. These findings suggest that VLDLR and ApoER2 participate in transmitting the extracellular Reelin signal to intracellular signaling processes initiated by mDab1.

摘要

大脑皮层和小脑神经元的分层需要细胞外基质蛋白Reelin以及哺乳动物Disabled(mDab1),mDab1是一种激活酪氨酸激酶的胞质蛋白。在此,我们报告另外两种蛋白质的需求,即称为极低密度脂蛋白受体(VLDLR)和载脂蛋白E受体2(ApoER2)的细胞表面受体。这两种受体都能在其细胞质尾部结合mDab1,并在与表达Reelin的层相邻的皮质层和小脑层中表达。在同时缺乏VLDLR和ApoER2的基因敲除小鼠中,mDab1的表达上调。这些动物中皮层层的倒置和小脑叶的缺失精确地模拟了缺乏Reelin或mDab1的小鼠的表型。这些发现表明,VLDLR和ApoER2参与将细胞外Reelin信号传递到由mDab1启动的细胞内信号传导过程。

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