Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease
about
Strategies for treatment in Alexander diseaseAlexander diseaseDysfunctions of neuronal and glial intermediate filaments in diseasePost-translational modifications of intermediate filament proteins: mechanisms and functionsIntracellular fibril formation, calcification, and enrichment of chaperones, cytoskeletal, and intermediate filament proteins in the adult hippocampus CA1 following neonatal exposure to the nonprotein amino acid BMAASuppression of neuroinflammation by astrocytic dopamine D2 receptors via αB-crystallinGFAP isoforms control intermediate filament network dynamics, cell morphology, and focal adhesions.The origin of Rosenthal fibers and their contributions to astrocyte pathology in Alexander diseaseComparison of the gene expression profiles of human fetal cortical astrocytes with pluripotent stem cell derived neural stem cells identifies human astrocyte markers and signaling pathways and transcription factors active in human astrocytesAlexander disease causing mutations in the C-terminal domain of GFAP are deleterious both to assembly and network formation with the potential to both activate caspase 3 and decrease cell viability.Astrocyte Dysfunction in Developmental Neurometabolic Diseases.Protein misfolding and oxidative stress promote glial-mediated neurodegeneration in an Alexander disease modelLithium Decreases Glial Fibrillary Acidic Protein in a Mouse Model of Alexander Disease.Neurological diseases as primary gliopathies: a reassessment of neurocentrismEffects of maternal immune activation on gene expression patterns in the fetal brainBeneficial effects of Nrf2 overexpression in a mouse model of Alexander disease.Study of αB-crystallin expression in Gerbil BCAO model of transient global cerebral ischemia.Nitric oxide mediates glial-induced neurodegeneration in Alexander diseaseAn In Vivo Pharmacological Screen Identifies Cholinergic Signaling as a Therapeutic Target in Glial-Based Nervous System Disease.Alzheimer disease periventricular white matter lesions exhibit specific proteomic profile alterationsProtein changes in immunodepleted cerebrospinal fluid from a transgenic mouse model of Alexander disease detected using mass spectrometryGFAP expression as an indicator of disease severity in mouse models of Alexander disease.Promotion of axon regeneration and inhibition of astrocyte activation by alpha A-crystallin on crushed optic nerve.αB-Crystallin overexpression in astrocytes modulates the phenotype of the BACHD mouse model of Huntington's diseaseProteins that mediate protein aggregation and cytotoxicity distinguish Alzheimer's hippocampus from normal controls.Composition of Rosenthal Fibers, the Protein Aggregate Hallmark of Alexander DiseaseSmall heat shock proteins mediate cell-autonomous and -nonautonomous protection in a Drosophila model for environmental-stress-induced degeneration.Caspase cleavage of GFAP produces an assembly-compromised proteolytic fragment that promotes filament aggregation.The protective and therapeutic function of small heat shock proteins in neurological diseases.Myelination: do astrocytes play a role?Emerging role of autophagy in pediatric neurodegenerative and neurometabolic diseases.ASTROCYTES: EMERGING STARS IN LEUKODYSTROPHY PATHOGENESIS.Regulation of αA- and αB-crystallins via phosphorylation in cellular homeostasis.Lessons from Animal Models of Cytoplasmic Intermediate Filament Proteins.Leukodystrophies: a proposed classification system based on pathological changes and pathogenetic mechanisms.Traumatically injured astrocytes release a proteomic signature modulated by STAT3-dependent cell survival.Chaperones: needed for both the good times and the bad times.Alexander Disease Mutations Produce Cells with Coexpression of Glial Fibrillary Acidic Protein and NG2 in Neurosphere Cultures and Inhibit Differentiation into Mature OligodendrocytesDemyelination during multiple sclerosis is associated with combined activation of microglia/macrophages by IFN-γ and alpha B-crystallin.Effects of a polymorphism in the GFAP promoter on the age of onset and ambulatory disability in late-onset Alexander disease.
P2860
Q24596794-F4E10956-0490-4B29-88C0-D7E107FC07D1Q24633313-9AADE578-42DB-425B-B41E-89F7D129E076Q24657653-C70924F2-BC08-4D51-9E03-64428E7AE5D7Q27004670-3F05EE18-BA68-43EF-BA05-6E67C6EE5D92Q28239546-168891CD-00C8-47C6-A7AA-247ABFF25EB3Q28510018-4D4FAF6B-C5F2-469F-9DA4-488E8367A3B6Q30816841-4BD31097-4B9C-42D0-AA92-58E2061D08B8Q30843456-9357FE8C-BC03-40AF-AF17-1D2DCF3B3EEBQ31161502-43D44A92-7FD4-466D-B76A-5AA2EC8E4ABFQ34200416-1FF0AB12-BF9E-4E83-94D3-68BC63FA6115Q34679071-1713B3E1-F0B9-4B09-9D59-E8316D3EC415Q34857360-78CF0985-EBAC-4391-B91F-47D0A0BB96E6Q35778386-D9D61CC9-6EC6-4EC5-AD75-3FA9F677519AQ35872654-D8A695EB-1779-4235-BC6B-6481A27D87C8Q35913929-91042EF1-B5CB-4598-92E1-0D3D21383E54Q36251679-AD2C579F-3068-477B-BF3C-272F695F988CQ36336732-DCB760B9-AF05-4E4C-9098-E5CFE24B989CQ36360991-28734452-DCB8-4992-980B-3F5E97BEE8A5Q36534299-884B32F2-8455-4039-9E91-264E85E38C50Q36597843-800E41C7-5872-4BE4-9C4B-0F9B431EDC3AQ36599253-789D64DB-C36A-4ED6-9C1F-31418C144BCAQ36706156-007674D8-41C9-41B1-BB86-35E606151CD4Q37110854-DEC128A1-8BF1-43B2-B03F-20D26E7A7E1EQ37178561-FE3FBE10-5D87-43CD-ABDA-D14887F84275Q37235572-25AF72B1-23D8-4CCD-82F8-562C26347358Q37284065-6EDA07AF-CC7D-4643-B06B-304DCE4F529AQ37305913-7241FB26-DADB-43B0-85F7-6E687C1E21B9Q37323740-CAB8C94A-B785-4793-8887-3DAED66EDA73Q38008372-896D9CEE-5561-4BA6-82AC-ABC0975C51DDQ38058202-F506B7D3-34BB-4098-8641-C60F71D8161DQ38156022-69146F58-B3C2-4E0C-96AB-5DA8C72CB427Q38171484-55778616-A2A1-4A11-B2FE-52EC810097ADQ38554083-773586DA-E0A9-4488-8830-7DF703B22638Q39094595-8F62CCEC-A2CC-43AA-93C8-FCE549FC9B9CQ39389823-E58696ED-16A2-4691-AFBB-F3B4E9E180DDQ39421531-5BCC217B-F354-439C-9406-92025FF4DAA9Q40183775-70F58D8B-898F-42AD-B37B-42C4B34609E9Q42220379-CAF99CE0-234B-4A67-BDA8-08B7930BDE4CQ44587763-39E7F38E-C302-4BFB-BB98-6003343C3396Q45406318-3AB93430-472A-462B-BE35-E734DD0FB0E0
P2860
Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 07 January 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease
@en
Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease.
@nl
type
label
Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease
@en
Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease.
@nl
prefLabel
Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease
@en
Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease.
@nl
P2093
P2860
P356
P1476
Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease
@en
P2093
Albee Messing
Eric F Wawrousek
Tracy L Hagemann
Wilbert C Boelens
P2860
P304
P356
10.1093/HMG/DDP013
P577
2009-01-07T00:00:00Z