Brain protein 4.1 subtypes: a working hypothesis.

Brain protein 4.1 subtypes: a working hypothesis.
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脑蛋白 4.1 亚型:一个可行的假设。

DOI:
10.1002/bies.950060607
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发表时间:
1987
期刊:
BioEssays : news and reviews in molecular, cellular and developmental biology
影响因子:
--
通讯作者:
Goodman,SR
Goodman,SR
中科院分区:
--
文献类型:
--
作者:
Krebs,KE;Zagon,IS;Sihag,R;Goodman,SR

文献摘要

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在一个伴随的综述中,我们讨论了支持以下结论的数据:在哺乳动物大脑中至少存在两种血影蛋白亚型。一种形式存在于神经元的细胞体、树突和突触后末梢(脑血影蛋白(240/235 E)),另一种亚型位于轴突和突触前末梢(脑血影蛋白(240/235))。我们最近的理解,脑血影蛋白亚型定位提出了一个可能的解释有关脑4.1定位的难题。釉蛋白是红细胞骨架蛋白4.1的免疫反应类似物,当用抗红细胞骨架蛋白4.1的抗体对脑切片进行染色时,釉蛋白定位于神经元细胞体和树突中。然而,最近有人提出突触蛋白I,一种与小突触囊泡的细胞质表面相关的神经元特异性磷蛋白,与红细胞4.1相关。在这篇综述中,我们假设至少有两种形式的脑4.1:一种是红细胞蛋白4.1抗体检测到的细胞体/树突状形式(amelin),另一种是突触前末端发现的独特形式(synapsin I)。突触蛋白I与脑血影蛋白(240/235)的结合及其以磷酸化依赖性方式刺激血影蛋白/F-肌动蛋白相互作用的能力表明了神经元细胞骨架介导的突触传递调节模型。
In a companion review1we discussed the data supporting the conclusion that at least two subtypes of spectrin exist in mammalian brain. One form is found in the cell bodies, dendrites, and post‐synaptic terminals of neurons (brain spectrin(240/235E)) and the other subtype is located in the axons and presynaptic terminals (brain spectrin(240/235)). Our recent understanding of brain spectrin subtype localization suggests a possible explanation for a conundrum concerning brain 4.1 localization. Amelin, an immunoreactive analogue of red blood cell (rbc) cytoskeletal protein 4.1, is localized in neuronal cell bodies and dendrites when brain sections are stained with antibody against rbc protein 4.1. However, it has recently been suggested that synapsin I, a neuron‐specific phosphoprotein associated with the cytoplasmic surface of small synaptic vesicles, is related to erythrocyte 4.1. In this review we hypothesize that there are at least two forms of brain 4.1: a cell body/dendritic form (amelin) which is detected with rbc protein 4.1 antibody, and a unique form found exclusively in the presynaptic terminal (synapsin I). The binding of synapsin I to brain spectrin(240/235), and its ability to stimulate the spectrin/F‐actin interaction in a phosphorylation‐dependent manner suggests a model for the regulation of synaptic transmission mediated by the neuronal cytoskeleton.