ArticleThe Journal of biological chemistry2017
Glial fibrillary acidic protein exhibits altered turnover kinetics in a mouse model of Alexander disease.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Alexander disease mutations differentially sensitize glial fibrillary acidic protein (GFAP) to posttranslational modifications and network disruption by oxidants.Redox biology · 2026Article
- Deciphering the Structural Biology of GFAP: Connotations of Its Potency in Presaging the Diagnosis for Traumatic Brain Injury and AD.Neurology international · 2025Review
- Induction of haemodynamic travelling waves by glial-related vasomotion in a rat model of neuroinflammation: implications for functional neuroimaging.EBioMedicine · 2025Article
- Gene therapy for the leukodystrophies: From preclinical animal studies to clinical trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- HIV Nef Expression Down-modulated GFAP Expression and Altered Glutamate Uptake and Release and Proliferation in Astrocytes.Aging and disease · 2023Article
- Redox-sensitive small GTPase H-Ras in murine astrocytes, anRedox report : communications in free radical research · 2022Article
- Alexander disease: models, mechanisms, and medicine.Current opinion in neurobiology · 2022Review
- Tau kinetics in Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Antisense therapy in a rat model of Alexander disease reverses GFAP pathology, white matter deficits, and motor impairment.Science translational medicine · 2021Article
- Bisulfite Amplicon Sequencing Can Detect Glia and Neuron Cell-Free DNA in Blood Plasma.Frontiers in molecular neuroscience · 2021Article
- Refining the concept of GFAP toxicity in Alexander disease.Journal of neurodevelopmental disorders · 2019Review
- Relative stabilities of wild-type and mutant glial fibrillary acidic protein in patients with Alexander disease.The Journal of biological chemistry · 2019Article
- Novel Insights on the Toxicity of Phycotoxins on the Gut through the Targeting of Enteric Glial Cells.Marine drugs · 2019Article
- Alexander disease: an astrocytopathy that produces a leukodystrophy.Brain pathology (Zurich, Switzerland) · 2018Review
- Astroglial vesicular network: evolutionary trends, physiology and pathophysiology.Acta physiologica (Oxford, England) · 2018Review
- Antisense suppression of glial fibrillary acidic protein as a treatment for Alexander disease.Annals of neurology · 2018Article
- Characterization of a panel of monoclonal antibodies recognizing specific epitopes on GFAP.PloS one · 2017Article
- GFAP at 50.ASN neuroReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
Mutations in the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP) lead to the rare and fatal disorder, Alexander disease (AxD). A prominent feature of the disease is aberrant accumulation of GFAP. It has been proposed that this accumulation occurs because of an increase in gene transcription coupled with impaired proteasomal degradation, yet this hypothesis remains untested. We therefore sought to directly investigate GFAP turnover in a mouse model of AxD that is heterozygous for a disease-causing point mutation (
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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.