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The neural cell adhesion molecule L1 potentiates integrin-dependent cell migration to extracellular matrix proteins
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Thelen K., Kedar V., Panicker A.K., Schmid R.S., Midkiff B.R., and Maness P.F. The neural cell adhesion molecule L1 potentiates integrin-dependent cell migration to extracellular matrix proteins. J Neurosci 22 (2002) 4918-4931
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Plasmin-sensitive dibasic sequences in the third fibronectin-like domain of L1-cell adhesion molecule (CAM) facilitate homomultimerization and concomitant integrin recruitment
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Silletti S., Mei F., Sheppard D., and Montgomery A.M. Plasmin-sensitive dibasic sequences in the third fibronectin-like domain of L1-cell adhesion molecule (CAM) facilitate homomultimerization and concomitant integrin recruitment. J Cell Biol 149 (2000) 1485-1502
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Adhesion molecule L1 stimulates neuronal migration through Vav2-Pak1 signaling
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Schmid R.S., Midkiff B.R., Kedar V.P., and Maness P.F. Adhesion molecule L1 stimulates neuronal migration through Vav2-Pak1 signaling. Neuroreport 15 (2004) 2791-2794
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A MAP kinase signaling pathway mediates neurite outgrowth on L1 and requires Src-dependent endocytosis
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Schmid R.S., Pruitt W.M., and Maness P.F. A MAP kinase signaling pathway mediates neurite outgrowth on L1 and requires Src-dependent endocytosis. J Neurosci 11 (2000) 4177-4188
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Schmid, R.S.1
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Extracellular signal-regulated kinase (ERK)-dependent gene expression contributes to L1 cell adhesion molecule-dependent motility and invasion
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Silletti S., Yebra M., Perez B., Cirulli V., McMahon M., and Montgomery A.M. Extracellular signal-regulated kinase (ERK)-dependent gene expression contributes to L1 cell adhesion molecule-dependent motility and invasion. J Biol Chem 279 (2004) 28880-28888
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MAP kinase pathway-dependent phosphorylation of the L1-CAM ankyrin binding site regulates neuronal growth
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Whittard J.D., Sakurai T., Cassella M.R., Gazdoiu M., and Felsenfeld D.P. MAP kinase pathway-dependent phosphorylation of the L1-CAM ankyrin binding site regulates neuronal growth. Mol Biol Cell 17 (2006) 2696-2706
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L1 interaction with ankyrin regulates mediolateral topography in the retinocollicular projection
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Buhusi M., Schlatter M.C., Demyanenko G.P., Thresher R., and Maness P.F. L1 interaction with ankyrin regulates mediolateral topography in the retinocollicular projection. J Neurosci 28 (2008) 177-188
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Buhusi, M.1
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Ankyrin-based subcellular gradient of neurofascin, an immunoglobulin family protein, directs GABAergic innervation at Purkinje axon initial segment
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The authors used BAC transgenic reporter mice expressing green fluorescent protein in an interneuron subpopulation to show that a subcellular gradient of the Neurofascin 186 isoform along the dendritic-somal-axon initial segment axis of cerebellar Purkinje cells is formed by the direct interaction with an ankyrin B isoform, and is responsible for axon targeting of basket interneurons to the axon initial segment. AnkyrinG-associated Neurofascin 186 is suggested to be required for the formation or stabilization of pinceau synapses at the axon initial segment.
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Ango F., di Cristo G., Higashiyama H., Bennett V., Wu P., and Huang Z.J. Ankyrin-based subcellular gradient of neurofascin, an immunoglobulin family protein, directs GABAergic innervation at Purkinje axon initial segment. Cell 119 (2004) 257-272. The authors used BAC transgenic reporter mice expressing green fluorescent protein in an interneuron subpopulation to show that a subcellular gradient of the Neurofascin 186 isoform along the dendritic-somal-axon initial segment axis of cerebellar Purkinje cells is formed by the direct interaction with an ankyrin B isoform, and is responsible for axon targeting of basket interneurons to the axon initial segment. AnkyrinG-associated Neurofascin 186 is suggested to be required for the formation or stabilization of pinceau synapses at the axon initial segment.
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Ango, F.1
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Close homolog of L1 modulates area-specific neuronal positioning and dendrite orientation in the cerebral cortex
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This study demonstrated for the first time a function for a cell adhesion molecule, CHL1, in cortical neuron migration and laminar positioning. CHL1 knockout mice were crossed with a fluorescent reporter strain (Thy1-YFP) to label layer V pyramidal neurons to reveal malpositioning of neurons to deeper layers specifically in caudal cortical areas (somatosensory and visual cortex) where CHL1 is normally expressed.
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Demyanenko G.P., Schachner M., Anton E., Schmid R., Feng G., Sanes J., and Maness P.F. Close homolog of L1 modulates area-specific neuronal positioning and dendrite orientation in the cerebral cortex. Neuron 44 (2004) 423-437. This study demonstrated for the first time a function for a cell adhesion molecule, CHL1, in cortical neuron migration and laminar positioning. CHL1 knockout mice were crossed with a fluorescent reporter strain (Thy1-YFP) to label layer V pyramidal neurons to reveal malpositioning of neurons to deeper layers specifically in caudal cortical areas (somatosensory and visual cortex) where CHL1 is normally expressed.
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Close homolog of L1 is an enhancer of integrin-mediated cell migration
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Buhusi M., Midkiff B.R., Gates A.M., Richter M., Schachner M., and Maness P.F. Close homolog of L1 is an enhancer of integrin-mediated cell migration. J Biol Chem 278 (2003) 25024-25031
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Schmid R.S., Jo R., Shelton S., Kreidberg J.A., and Anton E.S. Reelin, integrin and Dab1 interactions during embryonic cerebral cortical development. Cereb Cortex 15 (2005) 1632-1636
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Belvindrah R., Graus-Porta D., Goebbels S., Nave K.A., and Muller U. Beta1 integrins in radial glia but not in migrating neurons are essential for the formation of cell layers in the cerebral cortex. J Neurosci 27 (2007) 13854-13865
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Overlapping functions of the cell adhesion molecules Nr-CAM and L1 in cerebellar granule cell development
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Sakurai T., Lustig M., Babiarz J., Furley A.J., Tait S., Brophy P.J., Brown S.A., Brown L.Y., Mason C.A., and Grumet M. Overlapping functions of the cell adhesion molecules Nr-CAM and L1 in cerebellar granule cell development. J Cell Biol 154 (2001) 1259-1273
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Neural recognition molecules CHL1 and NB-3 regulate apical dendrite orientation in the neocortex via PTP alpha
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Ye H., Tan Y.L., Ponniah S., Takeda Y., Wang S.Q., Schachner M., Watanabe K., Pallen C.J., and Xiao Z.C. Neural recognition molecules CHL1 and NB-3 regulate apical dendrite orientation in the neocortex via PTP alpha. EMBO J 27 (2008) 188-200
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Fyn and Cdk5 mediate semaphorin-3A signaling, which is involved in regulation of dendrite orientation in cerebral cortex
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Sasaki Y., Cheng C., Uchida Y., Nakajima O., Ohshima T., Yagi T., Taniguchi M., Nakayama T., Kishida R., Kudo Y., et al. Fyn and Cdk5 mediate semaphorin-3A signaling, which is involved in regulation of dendrite orientation in cerebral cortex. Neuron 35 (2002) 907-920
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Chen G., Sima J., Jin M., Wang K.Y., Xue X.J., Zheng W., Ding Y.Q., and Yuan X.B. Semaphorin-3A guides radial migration of cortical neurons during development. Nat Neurosci 11 (2008) 36-44
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Close homolog of L1 and neuropilin 1 mediate guidance of thalamocortical axons at the ventral telencephalon
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Wright A.G., Demyanenko G.P., Powell A., Schachner M., Enriquez-Barreto L., Tran T.S., Polleux F., and Maness P.F. Close homolog of L1 and neuropilin 1 mediate guidance of thalamocortical axons at the ventral telencephalon. J Neurosci 27 (2007) 13667-13679
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Wright, A.G.1
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Analysis of the L1-deficient mouse phenotype reveals cross-talk between Sema3A and L1 signaling pathways in axonal guidance [see comments]
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This important work revealed a novel function for L1 in mediating repellent axon guidance and growth cone collapse to Sema3A. Using cocultures of cortical slices and spinal cord explants from wild-type and L1-minus mice, the authors demonstrate that this mechanism underlies repellent guidance of cortico-spinal tract axons in response to Sema3A in the ventral spinal cord, which may contribute guidance at the pyramidal decussation in vivo. It is also shown that L1 forms a stable cis-interacting complex with the Sema3A receptor Neuropilin-1, and that soluble L1 protein as a ligand converts the repulsive response into attraction.
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Castellani V., Chedotal A., Schachner M., Faivre-Sarrailh C., and Rougon G. Analysis of the L1-deficient mouse phenotype reveals cross-talk between Sema3A and L1 signaling pathways in axonal guidance [see comments]. Neuron 27 (2000) 237-249. This important work revealed a novel function for L1 in mediating repellent axon guidance and growth cone collapse to Sema3A. Using cocultures of cortical slices and spinal cord explants from wild-type and L1-minus mice, the authors demonstrate that this mechanism underlies repellent guidance of cortico-spinal tract axons in response to Sema3A in the ventral spinal cord, which may contribute guidance at the pyramidal decussation in vivo. It is also shown that L1 forms a stable cis-interacting complex with the Sema3A receptor Neuropilin-1, and that soluble L1 protein as a ligand converts the repulsive response into attraction.
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FAK-MAPK-dependent adhesion disassembly downstream of L1 contributes to semaphorin3A-induced collapse
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Bechara A., Nawabi H., Moret F., Yaron A., Weaver E., Bozon M., Abouzid K., Guan J.L., Tessier-Lavigne M., Lemmon V., et al. FAK-MAPK-dependent adhesion disassembly downstream of L1 contributes to semaphorin3A-induced collapse. EMBO J 27 (2008) 1549-1562
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Castellani V., De Angelis E., Kenwrick S., and Rougon G. Cis and trans interactions of L1 with neuropilin-1 control axonal responses to semaphorin 3A. EMBO J 21 (2002) 6348-6357
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FAK deficiency in cells contributing to the basal lamina results in cortical abnormalities resembling congenital muscular dystrophies
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Beggs H.E., Schahin-Reed D., Zang K., Goebbels S., Nave K.A., Gorski J., Jones K.R., Sretavan D., and Reichardt L.F. FAK deficiency in cells contributing to the basal lamina results in cortical abnormalities resembling congenital muscular dystrophies. Neuron 40 (2003) 501-514
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Rico B., Beggs H.E., Schahin-Reed D., Kimes N., Schmidt A., and Reichardt L.F. Control of axonal branching and synapse formation by focal adhesion kinase. Nat Neurosci 7 (2004) 1059-1069
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Niethammer P., Delling M., Sytnyk V., Dityatev A., Fukami K., and Schachner M. Cosignaling of NCAM via lipid rafts and the FGF receptor is required for neuritogenesis. J Cell Biol 157 (2002) 521-532
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Kolkova K., Novitskaya V., Pedersen N., Berezin V., and Bock E. Neural cell adhesion molecule-stimulated neurite outgrowth depends on activation of protein kinase C and the Ras-mitogen-activated protein kinase pathway. J Neurosci 20 (2000) 2238-2246
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The neural cell adhesion molecule NCAM is an alternative signaling receptor for GDNF family ligands
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The authors find that NCAM can act as a coreceptor for the GDNF receptor GFRα1 to activate FAK and Fyn signaling without the known GDNF signaling receptor RET. The NCAM-GFRα1 interaction downregulates NCAM-NCAM homophilic binding, suggesting that cis-interacting GFRα1 induces conformation changes in NCAM that regulates its ability to interact with different ligands.
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Paratcha G., Ledda F., and Ibanez C.F. The neural cell adhesion molecule NCAM is an alternative signaling receptor for GDNF family ligands. Cell 113 (2003) 867-879. The authors find that NCAM can act as a coreceptor for the GDNF receptor GFRα1 to activate FAK and Fyn signaling without the known GDNF signaling receptor RET. The NCAM-GFRα1 interaction downregulates NCAM-NCAM homophilic binding, suggesting that cis-interacting GFRα1 induces conformation changes in NCAM that regulates its ability to interact with different ligands.
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The authors generated PSA-negative, NCAM-positive mice by deletion of two polysialyltransferase genes, STX and PST, to reveal for the first time that loss of a glycan can be more important than loss of the glyco-conjugated protein for brain development. Loss of PSA caused a more severe phenotype of axonal tract defects, hydrocephalus, and lethality, which were rescued in a triple knockouts lacking NCAM. Thus, a major function of PSA is to mask NCAM function at certain times and places enabling NCAM contacts to form in an orderly manner.
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Weinhold B., Seidenfaden R., Rockle I., Muhlenhoff M., Schertzinger F., Conzelmann S., Marth J.D., Gerardy-Schahn R., and Hildebrandt H. Genetic ablation of polysialic acid causes severe neurodevelopmental defects rescued by deletion of the neural cell adhesion molecule. J Biol Chem 280 (2005) 42971-42977. The authors generated PSA-negative, NCAM-positive mice by deletion of two polysialyltransferase genes, STX and PST, to reveal for the first time that loss of a glycan can be more important than loss of the glyco-conjugated protein for brain development. Loss of PSA caused a more severe phenotype of axonal tract defects, hydrocephalus, and lethality, which were rescued in a triple knockouts lacking NCAM. Thus, a major function of PSA is to mask NCAM function at certain times and places enabling NCAM contacts to form in an orderly manner.
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Angata K., Huckaby V., Ranscht B., Terskikh A., Marth J.D., and Fukuda M. Polysialic acid-directed migration and differentiation of neural precursors are essential for mouse brain development. Mol Cell Biol 27 (2007) 6659-6668
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Di Cristo G., Chattopadhyaya B., Kuhlman S.J., Fu Y., Belanger M.C., Wu C.Z., Rutishauser U., Maffei L., and Huang Z.J. Activity-dependent PSA expression regulates inhibitory maturation and onset of critical period plasticity. Nat Neurosci 10 (2007) 1569-1577
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