Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter. - Wikidata - awgldk - TriplyDB

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

http://www.wikidata.org/entity/Q48579102

about

Connexin 43 astrocytopathy linked to rapidly progressive multiple sclerosis and neuromyelitis optica Systemic inflammation disrupts oligodendrocyte gap junctions and induces ER stress in a model of CNS manifestations of X-linked Charcot-Marie-Tooth disease.Extensive dysregulations of oligodendrocytic and astrocytic connexins are associated with disease progression in an amyotrophic lateral sclerosis mouse model.White matter astrocytes in health and disease.Regulation of gap junction channels by infectious agents and inflammation in the CNS.Microglia of prefrontal white matter in suicide Early disruption of glial communication via connexin gap junction in multiple sclerosis, Baló's disease and neuromyelitis optica.Adipocytes in both brown and white adipose tissue of adult mice are functionally connected via gap junctions: implications for Chagas disease.Activated immune response in an inherited leukodystrophy disease caused by the loss of oligodendrocyte gap junctions.Connexins-mediated glia networking impacts myelination and remyelination in the central nervous system.Mechanisms of white matter damage in multiple sclerosis.Autoimmune antigenic targets at the node of Ranvier in demyelinating disorders.Oligodendroglia: metabolic supporters of neurons.Endogenous repair and development inspired therapy of neurodegeneration in progressive multiple sclerosis.Increasing acetyl-CoA metabolism attenuates injury and alters spinal cord lipid content in mice subjected to experimental autoimmune encephalomyelitis.Connexins and their channels in inflammation.Connexins and pannexins: At the junction of neuro-glial homeostasis & disease.Mouse Hepatitis Virus Infection Remodels Connexin43-Mediated Gap Junction Intercellular Communication In Vitro and In Vivo.Microtubule-assisted altered trafficking of astrocytic gap junction protein connexin 43 is associated with depletion of connexin 47 during mouse hepatitis virus infection.Gene therapy targeting oligodendrocytes provides therapeutic benefit in a leukodystrophy model.Connexin43 and connexin47 alterations after neural precursor cells transplantation in experimental autoimmune encephalomyelitis.Remyelinating Pharmacotherapies in Multiple Sclerosis.A Unique TGFB1-Driven Genomic Program Links Astrocytosis, Low-Grade Inflammation and Partial Demyelination in Spinal Cord Periplaques from Progressive Multiple Sclerosis Patients.Function of Connexins in the Interaction between Glial and Vascular Cells in the Central Nervous System and Related Neurological Diseases.Differential loss of KIR4.1 immunoreactivity in multiple sclerosis lesions Connexin 30 Deficiency Attenuates Chronic but Not Acute Phases of Experimental Autoimmune Encephalomyelitis Through Induction of Neuroprotective Microglia

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Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

http://www.wikidata.org/entity/Q48579102

description

2012 nî lūn-bûn

@nan

2012年の論文

@ja

2012年学术文章

@wuu

2012年学术文章

@zh-cn

2012年学术文章

@zh-hans

2012年学术文章

@zh-my

2012年学术文章

@zh-sg

2012年學術文章

@yue

2012年學術文章

@zh

2012年學術文章

@zh-hant

name

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

@en

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

@nl

type

label

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

@en

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

@nl

prefLabel

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

@en

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

@nl

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S00401-012-0978-4

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Acta Neuropathologica

P1476

Gap junction pathology in multiple sclerosis lesions and normal-appearing white matter.

@en

P2093

Andreas Hadjisavvas

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

Federico Roncaroli

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Irene Sargiannidou

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Kleopas A Kleopa

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Kyriaki Markoullis

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Natasa Schiza

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Richard Reynolds

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P2860

Mutations in the gene encoding gap junction protein alpha 12 (connexin 46.6) cause Pelizaeus-Merzbacher-like disease

Connexin 43 (GJA1) mutations cause the pleiotropic phenotype of oculodentodigital dysplasia

Hereditary spastic paraplegia is a novel phenotype for GJA12/GJC2 mutations

Human oligodendrocytes express Cx31.3: function and interactions with Cx32 mutants

Connexin-47 and connexin-32 in gap junctions of oligodendrocyte somata, myelin sheaths, paranodal loops and Schmidt-Lanterman incisures: implications for ionic homeostasis and potassium siphoning.

Loss-of-function GJA12/Connexin47 mutations cause Pelizaeus-Merzbacher-like disease

Abnormal endothelial tight junctions in active lesions and normal-appearing white matter in multiple sclerosis

Distinct patterns of multiple sclerosis pathology indicates heterogeneity on pathogenesis

Multiple sclerosis

Connexin30 in rodent, cat and human brain: selective expression in gray matter astrocytes, co-localization with connexin43 at gap junctions and late developmental appearance

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s00401-012-0978-4

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873-886

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10.1007/S00401-012-0978-4

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6

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123

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Federico Roncaroli

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2012-04-07T00:00:00Z

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223965842

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multiple sclerosis