Glial fibrillary acidic protein exhibits altered turnover kinetics in a mouse model of Alexander disease
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Title
Glial fibrillary acidic protein exhibits altered turnover kinetics in a mouse model of Alexander disease
Authors
Keywords
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Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 292, Issue 14, Pages 5814-5824
Publisher
American Society for Biochemistry & Molecular Biology (ASBMB)
Online
2017-02-22
DOI
10.1074/jbc.m116.772020
References
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Related references
Note: Only part of the references are listed.- Composition of Rosenthal Fibers, the Protein Aggregate Hallmark of Alexander Disease
- (2016) Michael R. Heaven et al. JOURNAL OF PROTEOME RESEARCH
- Astrocytic TDP-43 Pathology in Alexander Disease
- (2014) A. K. Walker et al. JOURNAL OF NEUROSCIENCE
- Regulated protein turnover: snapshots of the proteasome in action
- (2014) Sucharita Bhattacharyya et al. NATURE REVIEWS MOLECULAR CELL BIOLOGY
- Post-translational modifications of intermediate filament proteins: mechanisms and functions
- (2014) Natasha T. Snider et al. NATURE REVIEWS MOLECULAR CELL BIOLOGY
- Human Traumatic Brain Injury Induces Autoantibody Response against Glial Fibrillary Acidic Protein and Its Breakdown Products
- (2014) Zhiqun Zhang et al. PLoS One
- Caspase Cleavage of GFAP Produces an Assembly-Compromised Proteolytic Fragment that Promotes Filament Aggregation
- (2013) Mei-Hsuan Chen et al. ASN Neuro
- GFAP Expression as an Indicator of Disease Severity in Mouse Models of Alexander Disease
- (2013) Paige L. Jany et al. ASN Neuro
- Bioactive 3D cell culture system minimizes cellular stress and maintains thein vivo-like morphological complexity of astroglial cells
- (2013) Till B. Puschmann et al. GLIA
- Beneficial Effects of Nrf2 Overexpression in a Mouse Model of Alexander Disease
- (2012) C. M. LaPash Daniels et al. JOURNAL OF NEUROSCIENCE
- 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
- (2011) Yi-Song Chen et al. EXPERIMENTAL CELL RESEARCH
- A Data Processing Pipeline for Mammalian Proteome Dynamics Studies Using Stable Isotope Metabolic Labeling
- (2011) Shenheng Guan et al. MOLECULAR & CELLULAR PROTEOMICS
- Multiple Oxygen Tension Environments Reveal Diverse Patterns of Transcriptional Regulation in Primary Astrocytes
- (2011) Wayne Chadwick et al. PLoS One
- Drug screening to identify suppressors of GFAP expression
- (2010) Woosung Cho et al. HUMAN MOLECULAR GENETICS
- 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
- (2010) Guomei Tang et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Strategies for treatment in Alexander disease
- (2010) Albee Messing et al. Neurotherapeutics
- Analysis of proteome dynamics in the mouse brain
- (2010) J. C. Price et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice
- (2008) Woosung Cho et al. EXPERIMENTAL CELL RESEARCH
- Autophagy induced by Alexander disease-mutant GFAP accumulation is regulated by p38/MAPK and mTOR signaling pathways
- (2008) G. Tang et al. HUMAN MOLECULAR GENETICS
- A Transcriptome Database for Astrocytes, Neurons, and Oligodendrocytes: A New Resource for Understanding Brain Development and Function
- (2008) J. D. Cahoy et al. JOURNAL OF NEUROSCIENCE
- Glial Fibrillary Acidic Protein Filaments Can Tolerate the Incorporation of Assembly-compromised GFAP-δ, but with Consequences for Filament Organization and αB-Crystallin Association
- (2008) Ming-Der Perng et al. MOLECULAR BIOLOGY OF THE CELL
- Adapting Proteostasis for Disease Intervention
- (2008) William E. Balch et al. SCIENCE
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