Multiple sclerosis: oligodendrocytes display cell death-related molecules in situ but do not undergo apoptosis.
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The pathology of multiple sclerosis and its evolutionNeuroprotection and remyelination after autoimmune demyelination in mice that inducibly overexpress CXCL1The extracellular matrix, p53 and estrogen compete to regulate cell-surface Fas/Apo-1 suicide receptor expression in proliferating embryonic cerebral cortical precursors, and reciprocally, Fas-ligand modifies estrogen control of cell-cycle proteinsInduction of tumor necrosis factor-alpha (TNF-alpha) by interleukin-12 p40 monomer and homodimer in microglia and macrophagesTemporal profiles of the subcellular localization of Bim, a BH3-only protein, during middle cerebral artery occlusion in miceHeterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelinationRole of calcium in nitric oxide-induced cytotoxicity: EGTA protects mouse oligodendrocytes.Importance of oligodendrocyte protection, BBB breakdown and inflammation for remyelination.Macrophage infiltration, but not apoptosis, is correlated with immune-mediated demyelination following murine infection with a neurotropic coronavirus.Apoptosis in human autoimmune diseases.Myelin basic protein induces neuron-specific toxicity by directly damaging the neuronal plasma membrane.Inflammation in the nervous system: the human perspective.Oligodendrocyte apoptosis and primary demyelination induced by local TNF/p55TNF receptor signaling in the central nervous system of transgenic mice: models for multiple sclerosis with primary oligodendrogliopathy.Activation of NF-kappaB and c-jun transcription factors in multiple sclerosis lesions. Implications for oligodendrocyte pathology.Age dependence of clinical and pathological manifestations of autoimmune demyelination. Implications for multiple sclerosis.CCR1+/CCR5+ mononuclear phagocytes accumulate in the central nervous system of patients with multiple sclerosis.Increased calpain expression in activated glial and inflammatory cells in experimental allergic encephalomyelitisDual role for Fas ligand in the initiation of and recovery from experimental allergic encephalomyelitis.The role of CD4+ T-cells in the development of MS.Role of cytokine p40 family in multiple sclerosisMultiple sclerosis: death receptor expression and oligodendrocyte apoptosis in established lesions.A targeted DNA vaccine encoding fas ligand defines its dual role in the regulation of experimental autoimmune encephalomyelitisNeuroprotective effects of the complement terminal pathway during demyelination: implications for oligodendrocyte survival.The human microbiome in multiple sclerosis: pathogenic or protective constituents?The complex world of oligodendroglial differentiation inhibitors.Apoptosis: why and how does it occur in biology?Oligodendrocytes and the early multiple sclerosis lesion.Inherited and acquired disorders of myelin: The underlying myelin pathology.XIAP protects oligodendrocytes against cell death in vitro but has no functional role in toxic demyelination.Structural dynamics of oligodendrocyte lysis by perforin in culture: relevance to multiple sclerosis.Apoptotic death following Fas activation in human oligodendrocyte hybrid cultures.Association of increased bcl-2 expression with rescue from tumor necrosis factor-alpha-induced cell death in the oligodendrocyte cell line OLN-93.Apoptosis, neurotrophic factors and neurodegeneration.Synergistic activity of interleukin-17 and tumor necrosis factor-α enhances oxidative stress-mediated oligodendrocyte apoptosis.Expression of Fas and Fas ligand after experimental traumatic brain injury in the rat.Disialoganglioside GD3 is released by microglia and induces oligodendrocyte apoptosis.Estrogen receptor-dependent and estrogen receptor-independent pathways for tamoxifen and 4-hydroxytamoxifen-induced programmed cell death.Fas and Fas-L expression in Huntington's disease and Parkinson's disease.Demyelination in primate autoimmune encephalomyelitis and acute multiple sclerosis lesions: a case for antigen-specific antibody mediation.FasL (CD95L, Apo1L) is expressed in the normal rat and human brain: evidence for the existence of an immunological brain barrier.
P2860
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P2860
Multiple sclerosis: oligodendrocytes display cell death-related molecules in situ but do not undergo apoptosis.
description
1997 nî lūn-bûn
@nan
1997年の論文
@ja
1997年学术文章
@wuu
1997年学术文章
@zh
1997年学术文章
@zh-cn
1997年学术文章
@zh-hans
1997年学术文章
@zh-my
1997年学术文章
@zh-sg
1997年學術文章
@yue
1997年學術文章
@zh-hant
name
Multiple sclerosis: oligodendr ...... but do not undergo apoptosis.
@en
Multiple sclerosis: oligodendr ...... but do not undergo apoptosis.
@nl
type
label
Multiple sclerosis: oligodendr ...... but do not undergo apoptosis.
@en
Multiple sclerosis: oligodendr ...... but do not undergo apoptosis.
@nl
prefLabel
Multiple sclerosis: oligodendr ...... but do not undergo apoptosis.
@en
Multiple sclerosis: oligodendr ...... but do not undergo apoptosis.
@nl
P356
P1433
P1476
Multiple sclerosis: oligodendr ...... but do not undergo apoptosis.
@en
P2093
P356
10.1002/ANA.410420113
P577
1997-07-01T00:00:00Z