ArticleGlia2013
Transgenic analysis of GFAP promoter elements.
Article in Glia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 42 citations in OpenAlex.
- Evolution of Concepts Regarding the Diagnostic and Prognostic Significance of Glial Fibrillary Acidic Protein (GFAP)-Positive Extracellular Vesicles.Biomedicines · 2026Review
- Transcriptional Profiling Defines Unique Subtypes of Transit Amplifying Neural Progenitors Within the Neonatal Mouse Subventricular Zone.Biomolecules · 2025Article
- The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025Review
- The impact of astrocytic NF-κB on healthy and Alzheimer's disease brains.Scientific reports · 2024Article
- Improving cell-specific recombination using AAV vectors in the murine CNS by capsid and expression cassette optimization.Molecular therapy. Methods & clinical development · 2024Article
- STAT3 Drives GFAP Accumulation and Astrocyte Pathology in a Mouse Model of Alexander Disease.Cells · 2023Article
- HIV Nef Expression Down-modulated GFAP Expression and Altered Glutamate Uptake and Release and Proliferation in Astrocytes.Aging and disease · 2023Article
- RNF7 inhibits apoptosis and sunitinib sensitivity and promotes glycolysis in renal cell carcinoma via the SOCS1/JAK/STAT3 feedback loop.Cellular & molecular biology letters · 2022Article
- Propofol Exposure Disturbs the Differentiation of Rodent Neural Stem Cells via an miR-124-3p/Sp1/Cdkn1b Axis.Frontiers in cell and developmental biology · 2020Article
- Effects of Neutralizing Antibody Production on AAV-PHP.B-Mediated Transduction of the Mouse Central Nervous System.Molecular neurobiology · 2019Article
- Endothelin-1 stimulates expression of cyclin D1 and S-phase kinase-associated protein 2 by activating the transcription factor STAT3 in cultured rat astrocytes.The Journal of biological chemistry · 2019Article
- AP-1 and the injury response of the GFAP gene.Journal of neuroscience research · 2019Article
- AP-1Communications biology · 2019Article
- Exploring the Role of Astroglial Glutamate Release and Association With Synapses in Neuronal Function and Behavior.Biological psychiatry · 2018Review
- Anticancer and Differentiation Properties of the Nitric Oxide Derivative of Lopinavir in Human Glioblastoma Cells.Molecules (Basel, Switzerland) · 2018Article
- Composition of Rosenthal Fibers, the Protein Aggregate Hallmark of Alexander Disease.Journal of proteome research · 2016Article
- Complement Peptide C3a Promotes Astrocyte Survival in Response to Ischemic Stress.Molecular neurobiology · 2016Article
- Non-viral liposome-mediated transfer of brain-derived neurotrophic factor across the blood-brain barrier.Neural regeneration research · 2016Article
- Astrocytic GAP43 Induced by the TLR4/NF-κB/STAT3 Axis Attenuates Astrogliosis-Mediated Microglial Activation and Neurotoxicity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Viral Vector-Based Dissection of Marmoset GFAP Promoter in Mouse and Marmoset Brains.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Transcriptional regulation of the glial fibrillary acidic protein gene (GFAP) is of interest because of its astrocyte specificity and its upregulation in response to CNS injuries. We have used a transgenic approach instead of cell transfection to identify promoter elements of the human GFAP gene, since previous observations show that GFAP transcription is regulated differently in transfected cultured cells from in the mouse. We previously showed that block mutation of enhancer regions spanning from bp -1488 to -1434 (the C1.1 segment) and -1443 to -1399 (C1.2) resulted in altered patterns of expression and loss of astrocyte specificity, respectively. This analysis has now been extended upstream to bp -1612 to -1489 (the B region), which previously has been shown especially important for expression. Block mutation of each of four contiguous sequences, which together span the B region, each decreased the level of transgene activity by at least 50%, indicating that multiple sites contribute to the transcriptional activity in a cooperative manner. Several of the block mutations also altered the brain region pattern of expression, astrocyte specificity and/or the developmental time course. Transgenes were then analyzed in which mutations were limited to specific transcription factor binding sites in each of the 4 B block segments as well as in C1.1 and C1.2. Whereas mutation of the conserved consensus AP-1 site unexpectedly had little effect on transgene expression; NFI, SP1, STAT3, and NF-κB were identified as having important roles in regulating the strength of GFAP promoter activity and/or its astrocyte specificity.
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.