Oligomers of Mutant Glial Fibrillary Acidic Protein (GFAP) Inhibit the Proteasome System in Alexander Disease Astrocytes, and the Small Heat Shock Protein αB-Crystallin Reverses the Inhibition-Reference-Cited by-同舟云学术

Oligomers of Mutant Glial Fibrillary Acidic Protein (GFAP) Inhibit the Proteasome System in Alexander Disease Astrocytes, and the Small Heat Shock Protein αB-Crystallin Reverses the Inhibition

Published:2010-04 Issue:14 Volume:285 Page:10527-10537
ISSN:0021-9258
Container-title:Journal of Biological Chemistry
language:en
Short-container-title:Journal of Biological Chemistry

Author:

Tang Guomei,Perng Ming D.,Wilk Sherwin,Quinlan Roy,Goldman James E.

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference33 articles.

1. Mutations in GFAP, encoding glial fibrillary acidic protein, are associated with Alexander disease

2. Glial fibrillary acidic protein mutations in infantile, juvenile, and adult forms of Alexander disease

3. Formation of GFAP Cytoplasmic Inclusions in Astrocytes and Their Disaggregation by αB-Crystallin

4. Alexander-disease mutation of GFAP causes filament disorganization and decreased solubility of GFAP

5. Synergistic Effects of the SAPK/JNK and the Proteasome Pathway on Glial Fibrillary Acidic Protein (GFAP) Accumulation in Alexander Disease

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