Activation of NF-kappaB and c-jun transcription factors in multiple sclerosis lesions. Implications for oligodendrocyte pathology.
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Microarray analysis of tumor necrosis factor alpha induced gene expression in U373 human glioblastoma cellsAdenosine A2A receptors modulate acute injury and neuroinflammation in brain ischemiaMyalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristicsMultiple sclerosis: molecular mechanisms and therapeutic opportunitiesDeletion of Jun proteins in adult oligodendrocytes does not perturb cell survival, or myelin maintenance in vivoNF-κB Pathways in the Pathogenesis of Multiple Sclerosis and the Therapeutic ImplicationsUse of cell permeable NBD peptides for suppression of inflammationIndirect down-regulation of nuclear NF-kappaB levels by cobalamin in the spinal cord and liver of the ratThe SWI/SNF chromatin-remodeling complex modulates peripheral T cell activation and proliferation by controlling AP-1 expression.Importance of oligodendrocyte protection, BBB breakdown and inflammation for remyelination.IkappaB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-kappaB in the central nervous systemA transcription factor map as revealed by a genome-wide gene expression analysis of whole-blood mRNA transcriptome in multiple sclerosis.SHP-1 deficiency and increased inflammatory gene expression in PBMCs of multiple sclerosis patients.Central neuroinvasion and demyelination by inflammatory macrophages after peripheral virus infection is controlled by SHP-1.Estradiol inhibits ongoing autoimmune neuroinflammation and NFkappaB-dependent CCL2 expression in reactive astrocytesNF-kappaB in neuronal plasticity and neurodegenerative disordersInterferon-γ activates nuclear factor-κ B in oligodendrocytes through a process mediated by the unfolded protein response.Glial cells as targets for cytotoxic immune mediators.Critical role for protein tyrosine phosphatase SHP-1 in controlling infection of central nervous system glia and demyelination by Theiler's murine encephalomyelitis virusEndogenous retrovirus-K promoter: a landing strip for inflammatory transcription factors?Oligodendrocyte-specific activation of PERK signaling protects mice against experimental autoimmune encephalomyelitis.Prodegenerative IκBα expression in oligodendroglial α-synuclein models of multiple system atrophy.GWAS analysis implicates NF-κB-mediated induction of inflammatory T cells in multiple sclerosis.Macrophages of multiple sclerosis patients display deficient SHP-1 expression and enhanced inflammatory phenotypeImmunomodulatory and anti-inflammatory effects of chondroitin sulphate.Interferon-beta treatment in multiple sclerosis attenuates inflammatory gene expression through inducible activity of the phosphatase SHP-1.Innate immunity in the pathogenesis of psoriasis.Novel NF-κB inhibitors: a patent review (2011 - 2014).Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis.NF-κB activation protects oligodendrocytes against inflammation.Cellular distribution of glucose and monocarboxylate transporters in human brain white matter and multiple sclerosis lesions.Integration of MicroRNA databases to study MicroRNAs associated with multiple sclerosis.JC virus agnoprotein inhibits in vitro differentiation of oligodendrocytes and promotes apoptosis.Laquinimod prevents cuprizone-induced demyelination independent of Toll-like receptor signalingSelective adenosine A2A receptor agonists and antagonists protect against spinal cord injury through peripheral and central effects.Calpain and calpastatin expression in primary oligodendrocyte culture: preferential localization of membrane calpain in cell processes.Allelic association of sequence variants in the herpes virus entry mediator-B gene (PVRL2) with the severity of multiple sclerosis.Selective adenosine A2a receptor antagonism reduces JNK activation in oligodendrocytes after cerebral ischaemia.Triptolide modulates T-cell inflammatory responses and ameliorates experimental autoimmune encephalomyelitis.Immunohistochemical localization of phosphorylated protein kinase R and phosphorylated eukaryotic initiation factor-2 alpha in the central nervous system of SJL mice with experimental allergic encephalomyelitis.
P2860
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P2860
Activation of NF-kappaB and c-jun transcription factors in multiple sclerosis lesions. Implications for oligodendrocyte pathology.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
Activation of NF-kappaB and c- ...... for oligodendrocyte pathology.
@ast
Activation of NF-kappaB and c- ...... for oligodendrocyte pathology.
@en
type
label
Activation of NF-kappaB and c- ...... for oligodendrocyte pathology.
@ast
Activation of NF-kappaB and c- ...... for oligodendrocyte pathology.
@en
prefLabel
Activation of NF-kappaB and c- ...... for oligodendrocyte pathology.
@ast
Activation of NF-kappaB and c- ...... for oligodendrocyte pathology.
@en
P2093
P2860
P1476
Activation of NF-kappaB and c- ...... for oligodendrocyte pathology
@en
P2093
P2860
P304
P356
10.1016/S0002-9440(10)65456-9
P407
P577
1999-11-01T00:00:00Z