Anti-GD1a antibodies activate complement and calpain to injure distal motor nodes of Ranvier in mice. - Wikidata - wikimedia - TriplyDB

Anti-GD1a antibodies activate complement and calpain to injure distal motor nodes of Ranvier in mice.

Anti-GD1a antibodies activate complement and calpain to injure distal motor nodes of Ranvier in mice.

http://www.wikidata.org/entity/Q48180410

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Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis Neuro-glial interactions at the nodes of Ranvier: implication in health and diseases Rapid and reversible responses to IVIG in autoimmune neuromuscular diseases suggest mechanisms of action involving competition with functionally important autoantibodies Node of Ranvier disruption as a cause of neurological diseases Fluorescently-tagged anti-ganglioside antibody selectively identifies peripheral nerve in living animals.Update on Guillain-Barré syndrome MMN: from immunological cross-talk to conduction block Antibodies to heteromeric glycolipid complexes in Guillain-Barré syndrome.Anti-Ganglioside Antibodies Induce Nodal and Axonal Injury via Fcγ Receptor-Mediated Inflammation.Dysfunction of nodes of Ranvier: a mechanism for anti-ganglioside antibody-mediated neuropathies.Anti-ganglioside antibody internalization attenuates motor nerve terminal injury in a mouse model of acute motor axonal neuropathy.Streptococcal IdeS: therapeutic potential for Guillain-Barré syndrome.Chronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype.Action mechanism of corticosteroids to aggravate Guillain-Barré syndrome.Anti-GM2 ganglioside antibodies are a biomarker for acute canine polyradiculoneuritis.Anti-ganglioside antibodies are removed from circulation in mice by neuronal endocytosis.Calpains mediate axonal cytoskeleton disintegration during Wallerian degeneration.Role of calpains in the injury-induced dysfunction and degeneration of the mammalian axon.Animal models of autoimmune neuropathy.Ganglioside deficiency causes inflammation and neurodegeneration via the activation of complement system in the spinal cord.The translation of the pathological findings described in humans to experimental models of acute motor axonal neuropathy.Recent developments and future directions in Guillain-Barré syndrome.Pharyngeal-cervical-brachial variant of Guillain-Barre syndrome.Pathophysiology of immune-mediated demyelinating neuropathies-part I: neuroscience.Pathophysiology of immune-mediated demyelinating neuropathies--Part II: Neurology.The node of Ranvier in multifocal motor neuropathy.Optimizing IgG therapy in chronic autoimmune neuropathies: a hypothesis driven approach.Nodopathies of the peripheral nerve: an emerging concept.Progress in inflammatory neuropathy -the legacy of Dr Jack Griffin.Serum Antibodies to Glycans in Peripheral Neuropathies.C1q-targeted inhibition of the classical complement pathway prevents injury in a novel mouse model of acute motor axonal neuropathy.Biological drugs in Guillain-Barré Syndrome: an update.Guillain-Barré syndrome: a century of progress.Autoantibody pathogenicity in a multifocal motor neuropathy induced pluripotent stem cell-derived model.Co-cultures with stem cell-derived human sensory neurons reveal regulators of peripheral myelination.The effects of age and ganglioside composition on the rate of motor nerve terminal regeneration following antibody-mediated injury in mice.The paranodal cytoskeleton clusters Na+ channels at nodes of Ranvier.Guillain-Barré syndrome in the 100 years since its description by Guillain, Barré and Strohl.Acute motor axonal neuropathy and multifocal motor neuropathy: more in common than not.Limb motor nerve dysfunction in Miller Fisher syndrome.

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Anti-GD1a antibodies activate complement and calpain to injure distal motor nodes of Ranvier in mice.

http://www.wikidata.org/entity/Q48180410

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2010 nî lūn-bûn

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2010年学术文章

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2010年学术文章

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2010年學術文章

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2010年學術文章

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Anti-GD1a antibodies activate ...... otor nodes of Ranvier in mice.

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Anti-GD1a antibodies activate ...... otor nodes of Ranvier in mice.

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Anti-GD1a antibodies activate ...... otor nodes of Ranvier in mice.

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Anti-GD1a antibodies activate ...... otor nodes of Ranvier in mice.

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Anti-GD1a antibodies activate ...... otor nodes of Ranvier in mice.

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P2093

Hugh J Willison

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Kay N Greenshields

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Koichi Furukawa

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Peter D Humphreys

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Russell P Rother

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P2860

The local differentiation of myelinated axons at nodes of Ranvier

Guillain-Barré syndrome

Sodium channel Na(v)1.6 is localized at nodes of ranvier, dendrites, and synapses

Traumatic axonal injury induces proteolytic cleavage of the voltage-gated sodium channels modulated by tetrodotoxin and protease inhibitors

Anti-GD1a antibody is associated with axonal but not demyelinating forms of Guillain-Barré syndrome

Heteromultimeric K+ channels in terminal and juxtaparanodal regions of neurons

Imaging neuronal subsets in transgenic mice expressing multiple spectral variants of GFP

Calpain mediates proteolysis of the voltage-gated sodium channel alpha-subunit.

Tolerance to self gangliosides is the major factor restricting the antibody response to lipopolysaccharide core oligosaccharides in Campylobacter jejuni strains associated with Guillain-Barré syndrome.

Does Campylobacter jejuni infection elicit "demyelinating" Guillain-Barre syndrome?

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1944-1960

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10.1093/BRAIN/AWQ119

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Pt 7

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133

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Rhona McGonigal

Susan K Halstead

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2010-05-30T00:00:00Z

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44640770

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20513658

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