ArticleHuman molecular genetics2010
Drug screening to identify suppressors of GFAP expression.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Review
- Research progress on biomarkers of traumatic brain injury.Animal models and experimental medicine · 2026Review
- Lung-Brain Axis-Generated Inflammatory Biomarkers in Traumatic Brain Injury and Acute Respiratory Distress Syndrome: Role of Mechanical Ventilation/Stress.Advances in biomarker sciences and technology · 2025Article
- Establishment and Use of Primary Cultured Astrocytes from Alexander Disease Model Mice.International journal of molecular sciences · 2024Article
- Prediction of clinical progression in nervous system diseases: plasma glial fibrillary acidic protein (GFAP).European journal of medical research · 2024Review
- Case report: Alexander's disease with "head drop" as the main symptom and literature review.Frontiers in neurology · 2022Article
- Beneficial Effect of Phenytoin and Carbamazepine onFrontiers in pharmacology · 2021Article
- Targeting and extending the eukaryotic druggable genome with natural products: cytoskeletal targets of natural products.Natural product reports · 2020Review
- Refining the concept of GFAP toxicity in Alexander disease.Journal of neurodevelopmental disorders · 2019Review
- Antisense suppression of glial fibrillary acidic protein as a treatment for Alexander disease.Annals of neurology · 2018Article
- 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
- Neuroprotection of Chrysanthemum indicum Linne against cerebral ischemia/reperfusion injury by anti-inflammatory effect in gerbils.Neural regeneration research · 2016Article
- CSF and Blood Levels of GFAP in Alexander DiseaseeNeuro · 2015Article
- Glial fibrillary acidic protein: from intermediate filament assembly and gliosis to neurobiomarker.Trends in neurosciences · 2015Review
- Bacopa monniera (CDRI-08) Upregulates the Expression of Neuronal and Glial Plasticity Markers in the Brain of Scopolamine Induced Amnesic Mice.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Finding degrees of separation: experimental approaches for astroglial and oligodendroglial cell isolation and genetic targeting.Journal of neuroscience methods · 2014Review
- GFAP expression as an indicator of disease severity in mouse models of Alexander disease.ASN neuro · 2013Article
- Ceftriaxone for Alexander's Disease: A Four-Year Follow-Up.JIMD reports · 2013Article
- Chronic psychosocial stress and citalopram modulate the expression of the glial proteins GFAP and NDRG2 in the hippocampus.Psychopharmacology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Glial fibrillary acidic protein (GFAP) is the major intermediate filament protein of astrocytes in the vertebrate central nervous system. Increased levels of GFAP are the hallmark feature of gliosis, a non-specific response of astrocytes to a wide variety of injuries and disorders of the CNS, and also occur in Alexander disease where the initial insult is a mutation within the coding region of GFAP itself. In both settings, excess GFAP may cause or exacerbate astrocyte dysfunction. With the goal of finding drugs that reduce the expression of GFAP, we have devised screens to detect changes in GFAP promoter activity or protein levels in primary cultures of mouse astrocytes in a 96-well format. We have applied these screens to libraries enriched in compounds that are already approved for human use by the FDA. We report that several compounds are active at micromolar levels in suppressing the expression of GFAP. Treatment of mice for 3 weeks with one of these drugs, clomipramine, causes nearly 50% reduction in the levels of GFAP protein in brain.
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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.