ArticleThe American journal of pathology1999
Formation of GFAP cytoplasmic inclusions in astrocytes and their disaggregation by alphaB-crystallin.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 84 citations in OpenAlex.
- Anastasis Drives Senescence and Non-Cell Autonomous Neurodegeneration in the Astrogliopathy Alexander Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions.Frontiers in cellular neuroscience · 2022Article
- Astrocyte-Oligodendrocyte-Microglia Crosstalk in Astrocytopathies.Frontiers in cellular neuroscience · 2020Review
- Localization of αA-Crystallin in Rat Retinal Müller Glial Cells and Photoreceptors.Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada · 2018Article
- Vanishing white matter: a leukodystrophy due to astrocytic dysfunction.Brain pathology (Zurich, Switzerland) · 2018Review
- Leukodystrophies: a proposed classification system based on pathological changes and pathogenetic mechanisms.Acta neuropathologica · 2017Review
- 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
- Article
- Crystallins and neuroinflammation: The glial side of the story.Biochimica et biophysica acta · 2016Article
- D-ribosylation induces cognitive impairment through RAGE-dependent astrocytic inflammation.Cell death & disease · 2014Article
- Caspase cleavage of GFAP produces an assembly-compromised proteolytic fragment that promotes filament aggregation.ASN neuro · 2013Article
- 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.Experimental cell research · 2011Article
- Multiple sites in αB-crystallin modulate its interactions with desmin filaments assembled in vitro.PloS one · 2011Article
- Strategies for treatment in Alexander disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2010Review
- 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.The Journal of biological chemistry · 2010Article
- Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice.Experimental cell research · 2009Article
- Suppression of GFAP toxicity by alphaB-crystallin in mouse models of Alexander disease.Human molecular genetics · 2009Article
- Glial fibrillary acidic protein filaments can tolerate the incorporation of assembly-compromised GFAP-delta, but with consequences for filament organization and alphaB-crystallin association.Molecular biology of the cell · 2008Article
- Autophagy induced by Alexander disease-mutant GFAP accumulation is regulated by p38/MAPK and mTOR signaling pathways.Human molecular genetics · 2008Article
- GFAP and its role in Alexander disease.Experimental cell research · 2007Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In several neuropathological conditions, alphaB-crystallin and glial fibrillary acidic protein (GFAP) accumulate and form cytoplasmic inclusions in astrocytes. To explore the pathogenesis of the inclusions and the possible functions of the accumulated alphaB-crystallin, GFAP and alphaB-crystallin were overexpressed in cultured astrocytes by transient transfection. Human GFAP formed filamentous, cytoplasmic inclusions in mouse astrocytes, NIH3T3 cells, rat C6 glioma cells, and human U251 glioma cells. These human GFAP inclusions did not contain the endogenous vimentin or beta-tubulin, and the intermediate filament and microtubular networks of the transfected cells appeared normal. alphaB-crystallin and hsp25 were associated with the GFAP inclusions. Increasing intracellular alphaB-crystallin levels using recombinant adenoviruses, either before or after GFAP inclusions were formed, decreased the number of inclusion-bearing astrocytes and converted the human GFAP from an inclusion to a spread, filamentous form. These results suggest that alphaB-crystallin reorganizes abnormal intermediate filament aggregates into the normal filamentous network.
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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.