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===Cadherin dependent migration===
Scaffold cell-dependent migration, in which neuronal cadherin (N-cadherin) adhesive molecules are tightly regulated, provides one mode of motility in developing neuron tissue. During cell migration, N-cadherin binds the neuron to a glial fiber, and allows for transfer of force, generated by an intracellular actin network treadmilling, to the glial fiber. Force transmission across the cell-[[glial cell|glial fiber]] interface sums over many individual N-cadherin/glial-fiber interactions, allowing required levels of traction force essential for migration. It has also been shown that these adhesive cadherin molecules are internalized, and recycled by the migratory neuron. This cadherin recycling mechanism is thought to be substantial in the neural adhesion-based migratory pathway.<ref>{{cite journal|last=Kawauchi|first=T|title=Cell Adhesion and Its Endocytic Regulation in Cell Migration during Neural Development and Cancer Metastasis|journal=International Journal of Molecular Sciences|year=2012|volume=13|series=4|pages=4564–4590|doi=10.3390/ijms13044564|doi-access=free}}</ref> Cadherin based migration is essential to tissue organization in the central nervous system, specifically in cortical layer formation.
It has also been sugguested that the N-cadherin pathway may be crucial in neuron [[Cell differentiation|differentiation]], as knockdown of the N-cadherin pathway leads to premature neuron differentiation.
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===Thy-1 adhesion protein===
Thy-1 (or [[thy-1|CD90.2]]) is a membrane bound [[glycoprotein]] that has been shown to be involved in the [[axon guidance]] pathway. This protein has been shown to be highly mobile, as it contains a [[Glycophosphatidylinositol|GPI]] membrane anchor. Although much of the details are elusive, it is known that thy-1 interacts with the protein dimer integrin found on [[astrocytes]], forming aggregates that can inhibit neurite outgrowth and extension. Thy-1 has also been shown to have involvement in the [[src (gene)|src]]-family kinase pathway.<ref>{{cite journal|last=Rege|first=Tanya|title=Thy-1, via its GPI anchor, modulates Src family kinase and focal adhesion kinase phosphorylation and subcellular localization, and fibroblast migration, in response to thrombospondin-1/hep I|journal=Chronology|year=2006|doi=10.1016/j.yexcr.2006.07.029|volume=312|pages=3752–3767}}</ref> This astrocyte-neuron feedback has been proposed as a mechanism involved in CNS tissue repair post-injury, as a down regulation of thy-1 may lead to enhanced neurite outgrowth. Additional research has shown that thy-1 expression in post natal humans is elevated for several weeks. This suggests that in addition to tissue repair, thy-1 might have roles in early CNS tissue development and organization.<ref>{{cite journal|last=Herrera-Molina|first=Rodrigo|title=Astrocytic aVb3 Integrin Inhibits Neurite Outgrowth and Promotes Retraction of Neuronal Processes by Clustering Thy-1|journal=PLoS ONE|date=May 2012|volume=7|series=3|pages=e34295|doi=10.1371/journal.pone.0034295|display-authors=etal|doi-access=free}}</ref><ref>{{cite journal|last=Barker|first=Thomas|title=Thy-1 regulates fibroblast focal adhesions, cytoskeletal organization and migration through modulation of p190 RhoGAP and Rho GTPase activity|journal=Experimental Cell Research|year=2004|volume=295|pages=488–496|doi=10.1016/j.yexcr.2004.01.026|pmid=15093746}}</ref>
===L1 family protein===
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