Oligodendrocyte-specific activation of PERK signaling protects mice against experimental autoimmune encephalomyelitis.
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Remyelination Therapy in Multiple SclerosisThe unfolded protein response in multiple sclerosisEndoplasmic Reticulum Stress Interacts With Inflammation in Human DiseasesInterferon Gamma: Influence on Neural Stem Cell Function in Neurodegenerative and Neuroinflammatory DiseaseMultiple Sclerosis and Obesity: Possible Roles of AdipokinesInhibition of colony-stimulating factor 1 receptor early in disease ameliorates motor deficits in SCA1 mice.Impaired eukaryotic translation initiation factor 2B activity specifically in oligodendrocytes reproduces the pathology of vanishing white matter disease in mice.PERK-dependent activation of JAK1 and STAT3 contributes to endoplasmic reticulum stress-induced inflammation.Pharmaceutical integrated stress response enhancement protects oligodendrocytes and provides a potential multiple sclerosis therapeuticImpaired eIF2B activity in ligodendrocytes contributes to VWMD pathogenesis.Pancreatic endoplasmic reticulum kinase activation promotes medulloblastoma cell migration and invasion through induction of vascular endothelial growth factor AcFLIP is critical for oligodendrocyte protection from inflammationMyelin Proteolipid Protein Complexes with αv Integrin and AMPA Receptors In Vivo and Regulates AMPA-Dependent Oligodendrocyte Progenitor Cell Migration through the Modulation of Cell-Surface GluR2 Expression.Inhibition of Vascular Endothelial Growth Factor Receptor 2 Exacerbates Loss of Lower Motor Neurons and Axons during Experimental Autoimmune Encephalomyelitis.ER Chaperone BiP/GRP78 Is Required for Myelinating Cell Survival and Provides Protection during Experimental Autoimmune Encephalomyelitis.Harnessing the integrated stress response for the treatment of multiple sclerosis.The role of the unfolded protein response in myelinationPerk Ablation Ameliorates Myelination in S63del-Charcot-Marie-Tooth 1B Neuropathy.Overexpression of CHOP in Myelinating Cells Does Not Confer a Significant Phenotype under Normal or Metabolic Stress Conditions.PERK activation preserves the viability and function of remyelinating oligodendrocytes in immune-mediated demyelinating diseasesNeuroprotective effects of vascular endothelial growth factor A in the experimental autoimmune encephalomyelitis model of multiple sclerosis.Dual role of the integrated stress response in medulloblastoma tumorigenesis.ER Dysfunction and Protein Folding Stress in ALS.Disturbance of endoplasmic reticulum proteostasis in neurodegenerative diseases.NF-κB signaling regulates myelination in the CNS.NF-κB activation protects oligodendrocytes against inflammation.ER stress and the unfolded protein response in neurodegeneration.Endoplasmic reticulum stress and the unfolded protein response in disorders of myelinating gliaPharmacological Inhibition of PERK Attenuates Early Brain Injury After Subarachnoid Hemorrhage in Rats Through the Activation of Akt.The integrated stress response.Endoplasmic Reticulum Protein Quality Control Failure in Myelin Disorders.Genetic inactivation of PERK signaling in mouse oligodendrocytes: normal developmental myelination with increased susceptibility to inflammatory demyelination.Neuroprotection by eIF2α-CHOP inhibition and XBP-1 activation in EAE/optic neuritiss.miR-219 Cooperates with miR-338 in Myelination and Promotes Myelin Repair in the CNS.The integrated stress response in hypoxia-induced diffuse white matter injury.Activating transcription factor 6α deficiency exacerbates oligodendrocyte death and myelin damage in immune-mediated demyelinating diseases.Atf6α deficiency suppresses microglial activation and ameliorates pathology of experimental autoimmune encephalomyelitis.PERK Pathway Activation Promotes Intracerebral Hemorrhage Induced Secondary Brain Injury by Inducing Neuronal Apoptosis Both in Vivo and in Vitro.Role of the unfolded protein response in organ physiology: lessons from mouse models.Role of nuclear factor κB in multiple sclerosis and experimental autoimmune encephalomyelitis
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Oligodendrocyte-specific activation of PERK signaling protects mice against experimental autoimmune encephalomyelitis.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
Oligodendrocyte-specific activ ...... autoimmune encephalomyelitis.
@en
type
label
Oligodendrocyte-specific activ ...... autoimmune encephalomyelitis.
@en
prefLabel
Oligodendrocyte-specific activ ...... autoimmune encephalomyelitis.
@en
P2093
P2860
P50
P1476
Oligodendrocyte-specific activ ...... autoimmune encephalomyelitis.
@en
P2093
Ali G Fenstermaker
Sharon W Way
Stephanie Jamison
Yifeng Lin
P2860
P304
P356
10.1523/JNEUROSCI.1636-12.2013
P407
P577
2013-04-01T00:00:00Z