Genetic deletion of the Nogo receptor does not reduce neurite inhibition in vitro or promote corticospinal tract regeneration in vivo. - sprookjes - yvandenbroek - TriplyDB

Genetic deletion of the Nogo receptor does not reduce neurite inhibition in vitro or promote corticospinal tract regeneration in vivo.

Genetic deletion of the Nogo receptor does not reduce neurite inhibition in vitro or promote corticospinal tract regeneration in vivo.

http://www.wikidata.org/entity/Q33724508

about

The reticulons: a family of proteins with diverse functions Myelin suppresses axon regeneration by PIR-B/SHP-mediated inhibition of Trk activity Oligodendrocyte-myelin glycoprotein and Nogo negatively regulate activity-dependent synaptic plasticity Glial inhibition of CNS axon regeneration Axon regeneration impediment: the role of paired immunoglobulin-like receptor B Growing the growth cone: remodeling the cytoskeleton to promote axon regeneration C. elegans as a genetic model to identify novel cellular and molecular mechanisms underlying nervous system regeneration Need for a paradigm shift in therapeutic approaches to CNS injury PlexinA2 limits recovery from corticospinal axotomy by mediating oligodendrocyte-derived Sema6A growth inhibition.Assessment of functional recovery and axonal sprouting in oligodendrocyte-myelin glycoprotein (OMgp) null mice after spinal cord injury Molecular basis of the interactions of the Nogo-66 receptor and its homolog NgR2 with myelin-associated glycoprotein: development of NgROMNI-Fc, a novel antagonist of CNS myelin inhibition LDL receptor-related protein-1 is a sialic-acid-independent receptor for myelin-associated glycoprotein that functions in neurite outgrowth inhibition by MAG and CNS myelin.The nogo receptor family restricts synapse number in the developing hippocampus NgR1 and NgR3 are receptors for chondroitin sulfate proteoglycans Nogo-receptors NgR1 and NgR2 do not mediate regulation of CD4 T helper responses and CNS repair in experimental autoimmune encephalomyelitis Characterizing the neurite outgrowth inhibitory effect of Mani.Critical period for acoustic preference in mice.Engineering neuronal growth cones to promote axon regeneration over inhibitory molecules.Glycan-dependent binding of galectin-1 to neuropilin-1 promotes axonal regeneration after spinal cord injury.Autophagy induction stabilizes microtubules and promotes axon regeneration after spinal cord injury.Analysis of axonal regeneration in the central and peripheral nervous systems of the NG2-deficient mouse.Inhibitory activity of myelin-associated glycoprotein on sensory neurons is largely independent of NgR1 and NgR2 and resides within Ig-Like domains 4 and 5 Soluble Nogo receptor down-regulates expression of neuronal Nogo-A to enhance axonal regeneration.Temporospatial expression and cellular localization of oligodendrocyte myelin glycoprotein (OMgp) after traumatic spinal cord injury in adult rats.Tuba1a gene expression is regulated by KLF6/7 and is necessary for CNS development and regeneration in zebrafish.The Nogo-Nogo receptor pathway limits a spectrum of adult CNS axonal growth.Functional axonal regeneration through astrocytic scar genetically modified to digest chondroitin sulfate proteoglycans.Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat Assessment of Nogo-66 receptor 1 function in vivo after spinal cord injury.Nogo-66 receptor antagonist peptide (NEP1-40) administration promotes functional recovery and axonal growth after lateral funiculus injury in the adult rat EphA4 deficient mice maintain astroglial-fibrotic scar formation after spinal cord injury.Ephrin-B3 is a myelin-based inhibitor of neurite outgrowth Blockade of Nogo receptor ligands promotes functional regeneration of sensory axons after dorsal root crush.Myelin-associated glycoprotein and its axonal receptors Traffic lights for axon growth: proteoglycans and their neuronal receptors.Mammalian target of rapamycin (mTOR) activation increases axonal growth capacity of injured peripheral nerves Genetic deletion and pharmacological inhibition of Nogo-66 receptor impairs cognitive outcome after traumatic brain injury in mice.Combined genetic attenuation of myelin and semaphorin-mediated growth inhibition is insufficient to promote serotonergic axon regeneration.Axon growth inhibition by RhoA/ROCK in the central nervous system.A selective Sema3A inhibitor enhances regenerative responses and functional recovery of the injured spinal cord.

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Genetic deletion of the Nogo receptor does not reduce neurite inhibition in vitro or promote corticospinal tract regeneration in vivo.

http://www.wikidata.org/entity/Q33724508

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Genetic deletion of the Nogo r ...... al tract regeneration in vivo.

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Genetic deletion of the Nogo r ...... al tract regeneration in vivo.

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Genetic deletion of the Nogo r ...... al tract regeneration in vivo.

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Genetic deletion of the Nogo r ...... al tract regeneration in vivo.

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Proceedings of the National Academy of Sciences of the United States of America

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Genetic deletion of the Nogo r ...... nal tract regeneration in vivo

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Binhai Zheng

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Carole Ho

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Jasvinder Atwal

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K Christopher Garcia

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Lauren Case

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Marc Tessier-Lavigne

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Xiao-lin He

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P2860

Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration

Structure and axon outgrowth inhibitor binding of the Nogo-66 receptor and related proteins

Structure of the Nogo receptor ectodomain: a recognition module implicated in myelin inhibition

A p75(NTR) and Nogo receptor complex mediates repulsive signaling by myelin-associated glycoprotein.

Nogo-66 receptor antagonist peptide promotes axonal regeneration

Oligodendrocyte-myelin glycoprotein is a Nogo receptor ligand that inhibits neurite outgrowth

Nogo-receptor gene activity: cellular localization and developmental regulation of mRNA in mice and humans

P75 interacts with the Nogo receptor as a co-receptor for Nogo, MAG and OMgp

Targeted mutation of the gene encoding the low affinity NGF receptor p75 leads to deficits in the peripheral sensory nervous system

Nogo-A and myelin-associated glycoprotein mediate neurite growth inhibition by antagonistic regulation of RhoA and Rac1

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