EPHB介导的前向信号
中文名称
通路描述
多个EPHB受体直接参与树突棘的发展和形态发生。这些受体更广泛地参与突触后发育，通过激活粘附激酶（FAK）和Rho家族GTP酶及其GEF发挥作用。树突棘形态发生是突触形成和成熟过程中大脑发育的重要部分。树突棘形态发生以纤毛缩短后形成成熟蘑菇状树突棘为特征（Moeller et al. 2006）。EPHBs通过调节肌动蛋白细胞骨架来控制神经元形态和运动。EPHBs通过相互作用与GTP交换因子（GEFs）如intersectin和kalirin来控制树突纤毛的运动，从而促进突触形成。EPHBs通过激活FAK，进而激活RHOA-ROCK-LIMK-1通路来抑制cofilin活性并抑制cofilin介导的树突棘重塑（Shi et al. 2009）。
英文描述
EPHB-mediated forward signaling Multiple EPHB receptors contribute directly to dendritic spine development and morphogenesis. These are more broadly involved in post-synaptic development through activation of focal adhesion kinase (FAK) and Rho family GTPases and their GEFs. Dendritic spine morphogenesis is a vital part of the process of synapse formation and maturation during CNS development. Dendritic spine morphogenesis is characterized by filopodia shortening followed by the formation of mature mushroom-shaped spines (Moeller et al. 2006). EPHBs control neuronal morphology and motility by modulation of the actin cytoskeleton. EPHBs control dendritic filopodia motility, enabling synapse formation. EPHBs exert these effects through interacting with the guanine exchange factors (GEFs) such as intersectin and kalirin. The intersectin-CDC42-WASP-actin and kalirin-RAC-PAK-actin pathways have been proposed to regulate the EPHB receptor mediated morphogenesis and maturation of dendritic spines in cultured hippocampal and cortical neurons (Irie & Yamaguchi 2002, Penzes et al. 2003). EPHBs are also involved in the regulation of dendritic spine morphology through FAK which activates the RHOA-ROCK-LIMK-1 pathway to suppress cofilin activity and inhibit cofilin-mediated dendritic spine remodeling (Shi et al. 2009).
所含基因
42 个基因