Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac. - Wikidata - awgldk - TriplyDB

Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

http://www.wikidata.org/entity/Q39430718

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Brain-Derived Neurotrophic Factor: Three Ligands, Many Actions A novel inhibitor of p75-neurotrophin receptor improves functional outcomes in two models of traumatic brain injury.Schwann cell interactions with axons and microvessels in diabetic neuropathy.The E3 ligase APC/C-Cdh1 is required for associative fear memory and long-term potentiation in the amygdala of adult mice Antipsychotics activate mTORC1-dependent translation to enhance neuronal morphological complexity p75NTR, but not proNGF, is upregulated following status epilepticus in mice.Dynamic plasticity: the role of glucocorticoids, brain-derived neurotrophic factor and other trophic factors.Small-molecule modulation of neurotrophin receptors: a strategy for the treatment of neurological disease.A cell-based fascin bioassay identifies compounds with potential anti-metastasis or cognition-enhancing functions.ProNGF promotes neurite growth from a subset of NGF-dependent neurons by a p75NTR-dependent mechanism The role of the retromer complex in aging-related neurodegeneration: a molecular and genomic review.HBpF-proBDNF: A New Tool for the Analysis of Pro-Brain Derived Neurotrophic Factor Receptor Signaling and Cell Biology Spatiotemporal patterns of sortilin and SorCS2 localization during organ development.Detection of p75NTR Trimers: Implications for Receptor Stoichiometry and Activation.ProNGF derived from rat sciatic nerves downregulates neurite elongation and axon specification in PC12 cells.Rare variants in the neurotrophin signaling pathway implicated in schizophrenia risk.Disruption of SorCS2 reveals differences in the regulation of stereociliary bundle formation between hair cell types in the inner ear.ProNGF, a cytokine induced after myocardial infarction in humans, targets pericytes to promote microvascular damage and activation Dependence of regenerated sensory axons on continuous neurotrophin-3 delivery Vps10 family proteins and the retromer complex in aging-related neurodegeneration and diabetes.Selective reduction of striatal mature BDNF without induction of proBDNF in the zQ175 mouse model of Huntington's disease Akt Regulates Axon Wrapping and Myelin Sheath Thickness in the PNS Of proneurotrophins and their antineurotrophic effects.Fascin regulates the migration of subventricular zone-derived neuroblasts in the postnatal brain.Shaping neurons: Long and short range effects of mature and proBDNF signalling upon neuronal structure.Val66Met polymorphism of BDNF alters prodomain structure to induce neuronal growth cone retraction Sympathetic denervation of peri-infarct myocardium requires the p75 neurotrophin receptor.Neurotrophin signalling: novel insights into mechanisms and pathophysiology.Pro-neurotrophins, sortilin, and nociception.Dynamic nature of the p75 neurotrophin receptor in response to injury and disease Fascin1 in carcinomas: Its regulation and prognostic value.Translational profiling of stress-induced neuroplasticity in the CA3 pyramidal neurons of BDNF Val66Met mice.Neurotrophic factors in Alzheimer's and Parkinson's diseases: implications for pathogenesis and therapy.Cellular and molecular mechanisms regulating neuronal growth by brain-derived neurotrophic factor.Growth factors and hormones pro-peptides: the unexpected adventures of the BDNF prodomain.New perspectives on the roles of Abl tyrosine kinase in axon patterning.Brain-Derived Neurotrophic Factor, Depression, and Physical Activity: Making the Neuroplastic Connection.Neuronal plasticity and neurotrophic factors in drug responses.Mir-592 regulates the induction and cell death-promoting activity of p75NTR in neuronal ischemic injury.proBDNF negatively regulates neuronal remodeling, synaptic transmission, and synaptic plasticity in hippocampus.

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Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

http://www.wikidata.org/entity/Q39430718

description

2011 nî lūn-bûn

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2011年の論文

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2011年学术文章

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2011年學術文章

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2011年學術文章

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2011年學術文章

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name

Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

@en

Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

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type

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Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

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Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

@nl

prefLabel

Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

@en

Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

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Science Signaling

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Neuronal growth cone retraction relies on proneurotrophin receptor signaling through Rac.

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Barbara L Hempstead

http://www.w3.org/2001/XMLSchema#string

Betty A Eipper

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Daniel S Spellman

http://www.w3.org/2001/XMLSchema#string

Richard E Mains

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Taeho Kim

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Thomas A Neubert

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P2860

Migrastatin analogues target fascin to block tumour metastasis

Sortilin is essential for proNGF-induced neuronal cell death

The multidomain protein Trio binds the LAR transmembrane tyrosine phosphatase, contains a protein kinase domain, and has separate rac-specific and rho-specific guanine nucleotide exchange factor domains

Identification of an actin binding region and a protein kinase C phosphorylation site on human fascin

Ephrin-B3 reverse signaling through Grb4 and cytoskeletal regulators mediates axon pruning

Molecular and Structural Insight into proNGF Engagement of p75NTR and Sortilin

Regulation of cell survival by secreted proneurotrophins.

Neurotrophin-induced melanoma cell migration is mediated through the actin-bundling protein fascin

The Human Rho-GEF trio and its target GTPase RhoG are involved in the NGF pathway, leading to neurite outgrowth

Continuous delta-opioid receptor activation reduces neuronal voltage-gated sodium channel (NaV1.7) levels through activation of protein kinase C in painful diabetic neuropathy

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202

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