Formation of GFAP cytoplasmic inclusions in astrocytes and their disaggregation by alphaB-crystallin.
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Strategies for treatment in Alexander diseaseGFAP and its role in Alexander diseaseD-ribosylation induces cognitive impairment through RAGE-dependent astrocytic inflammation.Alterations in the mouse and human proteome caused by Huntington's disease.Oligomers of mutant glial fibrillary acidic protein (GFAP) Inhibit the proteasome system in alexander disease astrocytes, and the small heat shock protein alphaB-crystallin reverses the inhibition.Autophagy induced by Alexander disease-mutant GFAP accumulation is regulated by p38/MAPK and mTOR signaling pathways.Small heat shock proteins, the cytoskeleton, and inclusion body formation.Multiple sites in αB-crystallin modulate its interactions with desmin filaments assembled in vitro.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.The Alexander disease-causing glial fibrillary acidic protein mutant, R416W, accumulates into Rosenthal fibers by a pathway that involves filament aggregation and the association of alpha B-crystallin and HSP27Crystallins and neuroinflammation: The glial side of the story.Glial fibrillary acidic protein filaments can tolerate the incorporation of assembly-compromised GFAP-delta, but with consequences for filament organization and alphaB-crystallin association.Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander diseaseCaspase cleavage of GFAP produces an assembly-compromised proteolytic fragment that promotes filament aggregation.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.A novel polymorphic AP-1 binding element of the GFAP promoter is associated with different allelic transcriptional activities.Mild functional effects of a novel GFAP mutant allele identified in a familial case of adult-onset Alexander disease.Redistribution of GFAP and alphaB-crystallin after thermal stress in C6 glioma cell line.Quantitative analysis of localization and nuclear aggregate formation induced by GFP-lamin A mutant proteins in living HeLa cells.Alexander Disease Mutations Produce Cells with Coexpression of Glial Fibrillary Acidic Protein and NG2 in Neurosphere Cultures and Inhibit Differentiation into Mature OligodendrocytesProperties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.p23 and HSP20/alpha-crystallin proteins define a conserved sequence domain present in other eukaryotic protein families.
P2860
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P2860
Formation of GFAP cytoplasmic inclusions in astrocytes and their disaggregation by alphaB-crystallin.
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
Formation of GFAP cytoplasmic ...... regation by alphaB-crystallin.
@ast
Formation of GFAP cytoplasmic ...... regation by alphaB-crystallin.
@en
type
label
Formation of GFAP cytoplasmic ...... regation by alphaB-crystallin.
@ast
Formation of GFAP cytoplasmic ...... regation by alphaB-crystallin.
@en
prefLabel
Formation of GFAP cytoplasmic ...... regation by alphaB-crystallin.
@ast
Formation of GFAP cytoplasmic ...... regation by alphaB-crystallin.
@en
P2860
P1476
Formation of GFAP cytoplasmic ...... regation by alphaB-crystallin.
@en
P2093
P2860
P304
P356
10.1016/S0002-9440(10)65409-0
P407
P577
1999-05-01T00:00:00Z