2017
DOI: 10.1111/tra.12473
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μ2‐Dependent endocytosis of N‐cadherin is regulated by β‐catenin to facilitate neurite outgrowth

Abstract: Circuit formation in the brain requires neurite outgrowth throughout development to establish synaptic contacts with target cells. Active endocytosis of several adhesion molecules facilitates the dynamic exchange of these molecules at the surface and promotes neurite outgrowth in developing neurons. The endocytosis of N-cadherin, a calcium-dependent adhesion molecule, has been implicated in the regulation of neurite outgrowth, but the mechanism remains unclear. Here, we identified that a fraction of N-cadherin… Show more

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Cited by 10 publications
(8 citation statements)
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“…The caveolin-mediated endocytic pathway, regulates the activity of signalling pathways such as WNT and TGFβ, both of which are known to play a central role in ESC pluripotency 23 25 . Endocytosis of CDH2 in an AP-2 adaptor complex dependent manner has been shown to be essential for neurite outgrowth and circuit formation 34 . Inhibition of RAB5 (early endosomal marker), or RAB11 (recycling endosome marker), showed defects in CDH2 trafficking, which resulted in neuronal migration defects during mouse cerebral cortex development 27 .…”
Section: Discussionmentioning
confidence: 99%
“…The caveolin-mediated endocytic pathway, regulates the activity of signalling pathways such as WNT and TGFβ, both of which are known to play a central role in ESC pluripotency 23 25 . Endocytosis of CDH2 in an AP-2 adaptor complex dependent manner has been shown to be essential for neurite outgrowth and circuit formation 34 . Inhibition of RAB5 (early endosomal marker), or RAB11 (recycling endosome marker), showed defects in CDH2 trafficking, which resulted in neuronal migration defects during mouse cerebral cortex development 27 .…”
Section: Discussionmentioning
confidence: 99%
“…This indicates that the cell adhesion may be decreased by the internalization of cadherins through clathrin-mediated endocytosis (CME). The µ2 subunit of the AP-2 adaptor complex interacts with several motifs of the intracellular domain of N-cadherin, and it is responsible for its endocytosis [20], while the β-catenin inhibits N-cadherin endocytosis by masking these motifs. The removal of β-catenin enables µ2 binding to N-cadherin, thereby increasing clathrin-mediated N-cadherin endocytosis in the neurite outgrowth.…”
Section: Cadherins-history and Functionmentioning
confidence: 99%
“…Upon LTD-inducing stimulation, AMPAR is sorted into clathrin-coated pits and efficiently removed from the plasma membrane, thereby reducing the sensitivity of neurons to neurotransmitters (Lee et al, 2002;Rosendale et al, 2017). During axon growth and before synapse formation, macropinocytosis, CME and an endophilin-dependent pathway (akin to FEME) are required to modulate attractive and repulsive receptors (Chen and Tai, 2017;Tojima and Kamiguchi, 2015;Chang et al, 2017). Finally, macropinocytosis mediates neuron-to-neuron transmission of protein aggregates, perhaps also supporting the spread of amyloids during neurodegenerative diseases (Yerbury, 2016).…”
Section: Endocytosis In Terminally Differentiated Cellsmentioning
confidence: 99%