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===Integrin dependent migration===
Integrin dependent cell migration can be described as protein plaques that form the mechanical linkage between the intracellular and extracellular environments. One major components of this classification of cell migration, [[integrin]], is a trans-membrenal protein dimer, which binds ECM components on its external domains and [[actin]] cytoskeletal components on its intra-cellular domains. These adhesions couple forces between the intracellular and extracellular space through both actin retrograde flow mechanisms (which have been described as a molecular clutch), and through actin-myosin protein contraction machinery. It is thought that these adhesions are involved in mechanosensing, that is, they respond both physically and chemically when exposed to various physical environments.<ref name="urlMechanosensitive channels">{{cite web | url = http://www.ks.uiuc.edu/Research/MscLchannel/ | title = Mechanosensitive channels |vauthors=Gullingsrud J, Sotomayor M
==Adhesion-related mechanisms involved in neuronal tissue development==
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==Relevant neurological conditions==
Several debilitating diseases are brought about from errors in neural development due in part to problems involving neural cell adhesions and adhesion mechanisms.
*CRASH syndrome (or L1 syndrome) is brought about by a mutation in the L1CAM gene on the x-[[chromosome]], resulting in a malfunctioning L1CAM protein. CRASH (acronym) syndrome include the conditions:<ref name="pmid8556302">{{cite journal |vauthors=Fransen E, Lemmon V, Van Camp G, Vits L, Coucke P, Willems PJ |title=CRASH syndrome: clinical spectrum of corpus callosum hypoplasia, retardation, adducted thumbs, spastic paraparesis and hydrocephalus due to mutations in one single gene, L1 |journal=European Journal of Human Genetics |volume=3 |issue=5 |pages=273–84 |year=1995 |pmid=8556302 |doi=10.1159/000472311 }}</ref><ref name="pmid7562969">{{cite journal |vauthors=Ruiz JC, Cuppens H, Legius E, etal |title=Mutations in L1-CAM in two families with X linked complicated spastic paraplegia, MASA syndrome, and HSAS |journal=Journal of Medical Genetics |volume=32 |issue=7 |pages=549–52 |date=July 1995 |pmid=7562969 |pmc=1050549 |doi= 10.1136/jmg.32.7.549
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