Amyloid Precursor Protein family as unconventional Go-coupled receptors and the control of neuronal motility.

Neurogenesis (Austin, Tex.) Pub Date : 2017-03-01 eCollection Date: 2017-01-01 DOI:10.1080/23262133.2017.1288510
Jenna M Ramaker, Philip F Copenhaver
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引用次数: 6

Abstract

Cleavage of the Amyloid Precursor Protein (APP) generates amyloid peptides that accumulate in Alzheimer Disease (AD), but APP is also upregulated by developing and injured neurons, suggesting that it regulates neuronal motility. APP can also function as a G protein-coupled receptor that signals via the heterotrimeric G protein Gαo, but evidence for APP-Gαo signaling in vivo has been lacking. Using Manduca as a model system, we showed that insect APP (APPL) regulates neuronal migration in a Gαo-dependent manner. Recently, we also demonstrated that Manduca Contactin (expressed by glial cells) induces APPL-Gαo retraction responses in migratory neurons, consistent with evidence that mammalian Contactins also interact with APP family members. Preliminary studies using cultured hippocampal neurons suggest that APP-Gαo signaling can similarly regulate growth cone motility. Whether Contactins (or other APP ligands) induce this response within the developing nervous system, and how this pathway is disrupted in AD, remains to be explored.

Abstract Image

Abstract Image

淀粉样前体蛋白家族作为非常规go偶联受体与神经元运动的控制。
淀粉样蛋白前体蛋白(APP)的切割产生淀粉样肽,在阿尔茨海默病(AD)中积累,但APP也在发育和损伤的神经元中上调,表明它调节神经元运动。APP也可以作为G蛋白偶联受体,通过异源三聚体G蛋白Gαo发出信号,但在体内缺乏APP-Gαo信号传导的证据。以Manduca为模型系统,我们发现昆虫APP (APPL)以g αo依赖的方式调节神经元迁移。最近,我们还发现Manduca Contactin(由神经胶质细胞表达)在迁移神经元中诱导APP - g - αo缩回反应,这与哺乳动物Contactins也与APP家族成员相互作用的证据一致。对培养海马神经元的初步研究表明,app - g - αo信号也可以类似地调节生长锥运动。接触物(或其他APP配体)是否在发育中的神经系统中诱导了这种反应,以及这一途径在AD中是如何被破坏的,仍有待探索。
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