app相关分子与p75NTR相互作用诱导的功能及信号通路

Y. Fujita, T. Yamashita
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引用次数: 0

摘要

p75神经营养因子受体(p75 NTR)通过与多种分子的关联,调控神经元的存活、分化、生长和凋亡等多种功能。越来越多的证据表明,调节多种神经元功能的β-淀粉样蛋白前体蛋白(APP)相关分子与p75 NTR相互作用。APP被分泌酶裂解生成多种蛋白,包括可溶性β-淀粉样蛋白前体蛋白α (sAPPα)、sAPPβ和淀粉样蛋白β (Aβ)。Aβ与p75 NTR结合可诱导神经元死亡。相反,sAPPα直接与p75 NTR相互作用,通过激活蛋白激酶A (PKA)来促进神经突生长。本文综述了p75 NTR与app相关分子相互作用的分子机制和功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The functions and signaling pathways induced by the interactions of APP–related molecules with p75NTR
p75 neurotrophin receptor (p75 NTR ) regulates diverse functions, including survival, differentiation, growth, and apoptosis of neurons, through its association with a number of molecules. Accumulating evidence shows that β-amyloid precursor protein (APP)–related molecules, which also regulate multiple neuronal functions, interact with p75 NTR . APP is cleaved by secretases to generate several proteins including soluble β-amyloid precursor protein alpha (sAPPα), sAPPβ, and amyloid β (Aβ). Binding of Aβ to p75 NTR induces neuronal death. In contrast, sAPPα directly interacts with p75 NTR to enhance neurite outgrowth through the activation of protein kinase A (PKA). This review focuses on the molecular mechanisms and functions occurring as a consequence of interactions of p75 NTR with APP–related molecules.
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