ArticleExperimental cell research2009
Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.
Article in Experimental cell research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- Synergistic Effects of Glial Fibrillary Acidic Protein Mutation and Overexpression in the Pathogenesis of Alexander Disease.International journal of molecular sciences · 2026Article
- Ranolazine neuroprotection against middle cerebral artery occlusion/reperfusion ischemic injury via modulation of brain-derived neurotrophic factor and brain mitochondrial tu translation elongation factor (TUFM).Metabolic brain disease · 2025Article
- Article
- PFOS Elicits Cytotoxicity in Neuron Through Astrocyte-Derived CaMKII-DLG1 Signaling In Vitro Rat Hippocampal Model.Neurochemical research · 2024Article
- Identification of association fibers using ex vivo diffusion tractography in Alexander disease brains.Journal of neuroimaging : official journal of the American Society of Neuroimaging · 2022Article
- Antisense therapy in a rat model of Alexander disease reverses GFAP pathology, white matter deficits, and motor impairment.Science translational medicine · 2021Article
- Role of astroglial Connexin 43 in pneumolysin cytotoxicity and during pneumococcal meningitis.PLoS pathogens · 2020Article
- Tissue and cellular rigidity and mechanosensitive signaling activation in Alexander disease.Nature communications · 2018Article
- Alexander disease: an astrocytopathy that produces a leukodystrophy.Brain pathology (Zurich, Switzerland) · 2018Review
- Leukodystrophies: a proposed classification system based on pathological changes and pathogenetic mechanisms.Acta neuropathologica · 2017Review
- Glial fibrillary acidic protein exhibits altered turnover kinetics in a mouse model of Alexander disease.The Journal of biological chemistry · 2017Article
- Alexander Disease Mutations Produce Cells with Coexpression of Glial Fibrillary Acidic Protein and NG2 in Neurosphere Cultures and Inhibit Differentiation into Mature Oligodendrocytes.Frontiers in neurology · 2017Article
- Characterization of a panel of monoclonal antibodies recognizing specific epitopes on GFAP.PloS one · 2017Article
- The role of gigaxonin in the degradation of the glial-specific intermediate filament protein GFAP.Molecular biology of the cell · 2016Article
- GFAP isoforms control intermediate filament network dynamics, cell morphology, and focal adhesions.Cellular and molecular life sciences : CMLS · 2016Article
- Modeling Alexander disease with patient iPSCs reveals cellular and molecular pathology of astrocytes.Acta neuropathologica communications · 2016Article
- Article
- Type 1 equilibrative nucleoside transporter regulates astrocyte-specific glial fibrillary acidic protein expression in the striatum.Brain and behavior · 2014Article
- The ubiquitin proteasome system in glia and its role in neurodegenerative diseases.Frontiers in molecular neuroscience · 2014Review
- Caspase cleavage of GFAP produces an assembly-compromised proteolytic fragment that promotes filament aggregation.ASN neuro · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alexander disease is a fatal leukoencephalopathy caused by dominantly-acting coding mutations in GFAP. Previous work has also implicated elevations in absolute levels of GFAP as central to the pathogenesis of the disease. However, identification of the critical astrocyte functions that are compromised by mis-expression of GFAP has not yet been possible. To provide new tools for investigating the nature of astrocyte dysfunction in Alexander disease, we have established primary astrocyte cultures from two mouse models of Alexander disease, a transgenic that over-expresses wild type human GFAP, and a knock-in at the endogenous mouse locus that mimics a common Alexander disease mutation. We find that mutant GFAP, as well as excess wild type GFAP, promotes formation of cytoplasmic inclusions, disrupts the cytoskeleton, decreases cell proliferation, increases cell death, reduces proteasomal function, and compromises astrocyte resistance to stress.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.