Essential roles for the FE65 amyloid precursor protein‐interacting proteins in brain development
作者： Suzanne Guénette , Yang Chang , Thomas Hiesberger , James A Richardson , Christopher B Eckman
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摘要: Targeted deletion of two members the FE65 family adaptor proteins, and FE65L1, results in cortical dysplasia. Heterotopias resembling those found cobblestone lissencephalies which neuroepithelial cells migrate into superficial layers developing cortex, aberrant projections loss infrapyramidal mossy fibers arise FE65/FE65L1 compound null animals, but not single gene knockouts. The disruption pial basal membranes underlying heterotopias poor organization fibrillar laminin by isolated meningeal fibroblasts from double knockouts suggests that proteins are involved basement membrane assembly. A similar phenotype is observed triple mutant mice lacking APP APP, APLP1 APLP2, all interact with suggesting this may be caused decreased transmission an APP-dependent signal through proteins. defects knockout also involve Ena/Vasp participate actin cytoskeleton remodeling WW domains
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