Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
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Strategies for treatment in Alexander diseaseAlexander diseaseDysfunctions of neuronal and glial intermediate filaments in diseaseThe ubiquitin proteasome system in glia and its role in neurodegenerative diseasesGFAP isoforms control intermediate filament network dynamics, cell morphology, and focal adhesions.Drug screening to identify suppressors of GFAP expressionKnockdown of MLC1 in primary astrocytes causes cell vacuolation: a MLC disease cell model.Characterization of a panel of monoclonal antibodies recognizing specific epitopes on GFAP.Alexander 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.Type 1 equilibrative nucleoside transporter regulates astrocyte-specific glial fibrillary acidic protein expression in the striatum.Neurological diseases as primary gliopathies: a reassessment of neurocentrismElevated GFAP induces astrocyte dysfunction in caudal brain regions: A potential mechanism for hindbrain involved symptoms in type II Alexander disease.GFAP expression as an indicator of disease severity in mouse models of Alexander disease.Modeling Alexander disease with patient iPSCs reveals cellular and molecular pathology of astrocytes.Caspase cleavage of GFAP produces an assembly-compromised proteolytic fragment that promotes filament aggregation.The role of gigaxonin in the degradation of the glial-specific intermediate filament protein GFAP.ASTROCYTES: EMERGING STARS IN LEUKODYSTROPHY PATHOGENESIS.Glial fibrillary acidic protein exhibits altered turnover kinetics in a mouse model of Alexander disease.Leukodystrophies: a proposed classification system based on pathological changes and pathogenetic mechanisms.Phenotypic conversions of "protoplasmic" to "reactive" astrocytes in Alexander disease.Alexander Disease Mutations Produce Cells with Coexpression of Glial Fibrillary Acidic Protein and NG2 in Neurosphere Cultures and Inhibit Differentiation into Mature OligodendrocytesTissue and cellular rigidity and mechanosensitive signaling activation in Alexander disease.
P2860
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P2860
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
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2008年學術文章
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name
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
@en
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
@nl
type
label
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
@en
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
@nl
prefLabel
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
@en
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
@nl
P2860
P1476
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
@en
P2093
Albee Messing
Woosung Cho
P2860
P304
P356
10.1016/J.YEXCR.2008.12.012
P407
P577
2008-12-29T00:00:00Z