Affinage

GFAP

Glial fibrillary acidic protein · UniProt P14136

Length
432 aa
Mass
49.9 kDa
Annotated
2026-06-10
100 papers in source corpus 27 papers cited in narrative 27 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GFAP is the principal type III intermediate filament protein of differentiated CNS astrocytes, forming the glial cytoskeleton that defines and maintains astrocyte shape (PMID:2409105). Its assembly into 10 nm filaments builds a dynamic network whose subunit exchange and organization are isoform-dependent: GFAPδ exchanges more slowly than GFAPα and shifting the isoform ratio reorganizes the network, alters focal adhesion size and cell morphology (PMID:27141937), and reprograms extracellular matrix engagement—changing plectin, laminin, and integrin levels to control adhesion and motility (PMID:24696300). Beyond structural support, the GFAP/vimentin filament system regulates astrocyte signaling competence, tuning Notch signal-sending capacity (PMID:26118771) and contributing to hippocampal circuit plasticity underlying memory extinction (PMID:31063456). GFAP expression is tightly controlled at a defined astrocyte-specific promoter (PMID:8120611, PMID:23832770) through a developmental switch in which repressive MeCP2/SIN3A occupancy gives way to STAT3 recruitment of CBP/p300 and activating histone modifications (PMID:21779366), and is further modulated by growth-factor and neurotransmitter inputs (TGF-β1 induction opposed by FGF-2; glutamate acting via mGluR2/3-TGF-β1-Smad signaling) (PMID:9537840, PMID:18419760). Post-translationally, GFAP is palmitoylated at cysteine-291 and depalmitoylated by PPT1; hyperpalmitoylation drives astrocyte proliferation, astrogliosis, and neurodegeneration, which is attenuated by the C291A mutation (PMID:33753498). Dominant de novo missense mutations in GFAP cause Alexander disease through a gain-of-function mechanism (PMID:12175861): mutant (or excess) GFAP disorganizes the filament network and becomes detergent-insoluble (PMID:15840648), forming Rosenthal-fiber inclusions that sequester the chaperones αB-crystallin and HSP27, activate JNK stress signaling, and impair proteasome function (PMID:17498694, PMID:19146851), and in patient iPSC-derived astrocytes disrupt ER and lysosome morphology, ATP release, and calcium wave propagation (PMID:30355500).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1985 High

    Established the founding identity of GFAP as the structural intermediate filament protein that builds the astrocyte cytoskeleton, defining the molecular basis of astrocyte shape.

    Evidence Biochemical and immunocytochemical characterization of glial filaments in CNS astrocytes

    PMID:2409105

    Open questions at the time
    • Does not address regulation of expression
    • Does not address assembly dynamics or post-translational control
  2. 1989 Medium

    Showed GFAP expression is not constitutive but dynamically driven by extrinsic cues, including trophic and developmental inputs, rather than being a fixed cell marker.

    Evidence dbcAMP labeling of astrocyte cultures; sciatic nerve transection with mRNA readout; insulin-titrated organotypic cerebellar cultures; pulse-chase turnover kinetics

    PMID:1782546 PMID:2279327 PMID:2769798 PMID:2989328

    Open questions at the time
    • Did not identify the promoter elements or transcription factors mediating these responses
    • Mechanism linking signal to GFAP transcription unresolved
  3. 1994 High

    Localized the regulatory logic of astrocyte-specific and injury-induced GFAP expression to a defined 5'-flanking promoter region, enabling dissection of its control elements.

    Evidence GFAP-promoter-lacZ transgenic mice with injury challenge

    PMID:8120611

    Open questions at the time
    • Did not resolve which transcription factors bind which elements
    • Did not address chromatin-level regulation
  4. 2002 High

    Defined Alexander disease as a dominant gain-of-function disorder of GFAP, distinguishing toxic-intermediate accumulation from simple loss of filament function.

    Evidence Mutation sequencing across patient cohorts; epistatic comparison with GFAP-null mice

    PMID:12175861

    Open questions at the time
    • Did not define the molecular nature of the toxic species
    • Did not link mutations to downstream cellular dysfunction
  5. 2005 High

    Resolved that disease mutations act on network organization and solubility rather than on filament polymerization, and connected progenitor signaling to GFAP+ cell identity.

    Evidence R239C transfection across cell lines with Triton-X-100 extraction and in vitro filament assembly; LIF/BMP treatment and transgenic BMP modulation of SVZ progenitors

    PMID:15840648 PMID:16314487

    Open questions at the time
    • Did not identify the chaperone or stress pathways engaged by insoluble mutant GFAP
    • GFAP+ progenitor heterogeneity not molecularly resolved
  6. 2008 Medium

    Built a cellular pathogenic model linking mutant/excess GFAP accumulation to chaperone sequestration, JNK stress activation, proteasome impairment, and reduced astrocyte viability.

    Evidence Review synthesis plus primary chaperone co-localization and JNK assays; primary astrocytes from GFAP-overexpressing and R236H knock-in mice with proteasome and stress assays

    PMID:17498694 PMID:19146851

    Open questions at the time
    • Causal order of chaperone sequestration vs JNK activation not established
    • Did not address organelle or secretory dysfunction
  7. 2008 Medium

    Mapped the transcriptional control of GFAP to discrete promoter elements and signaling inputs, establishing combinatorial astrocyte-specific and region-specific regulation.

    Evidence Transgenic promoter deletion/mutation analysis defining neuronal-silencer (C1.2) and region-specific (C1.1) elements and NFI/SP1/STAT3/NF-κB sites; reporter dissection of glutamate-mGluR2/3-TGF-β1-Smad activation

    PMID:18240313 PMID:18419760 PMID:23832770

    Open questions at the time
    • Did not establish chromatin-state dynamics during differentiation
    • Quantitative contribution of each factor in vivo not fully resolved
  8. 2011 High

    Defined the epigenetic switch driving GFAP induction during astrocyte differentiation, converting a repressed promoter into an active one via chromatin remodeling.

    Evidence ChIP for MeCP2/SIN3A, STAT3, CBP/p300, Pol II and histone marks in differentiating NTera-2 cells; MeCP2 siRNA in developing rat brain; HDAC inhibitor and SR-protein studies

    PMID:21779366 PMID:24269336 PMID:25128567

    Open questions at the time
    • Upstream trigger for SIN3A-MeCP2 departure not defined
    • Link between histone acetylation state and isoform splicing only partially resolved
  9. 2014 Medium

    Demonstrated that GFAP isoforms are functionally non-equivalent, with the GFAPα/GFAPδ ratio controlling network exchange dynamics, focal adhesions, ECM engagement, and motility.

    Evidence Isoform-specific shRNA silencing with adhesion/migration/integrin assays; FRAP of tagged GFAPα vs GFAPδ with morphology readouts

    PMID:24696300 PMID:27141937

    Open questions at the time
    • Mechanism coupling filament exchange to focal-adhesion remodeling unresolved
    • Relevance of isoform balance in vivo not established
  10. 2018 High

    Showed in a human isogenic system that disease-mutant GFAP disrupts organelle morphology and astrocyte secretory function, extending pathogenesis beyond filament aggregation to ER/lysosome and ATP/calcium signaling defects.

    Evidence iPSC-derived AxD astrocytes with isogenic correction; RNA-seq, organelle imaging, ATP release and calcium imaging assays

    PMID:30355500

    Open questions at the time
    • Mechanism linking filament aggregates to organelle enlargement not defined
    • Did not address therapeutic reversibility
  11. 2019 Medium

    Revealed signaling and behavioral roles of the astrocyte intermediate filament system beyond structure, including Notch signal-sending competence and hippocampal circuit plasticity.

    Evidence GFAP-/-Vim-/- mice with single-cell RT-qPCR and lesion model; behavioral battery including IntelliCage reversal learning

    PMID:26118771 PMID:31063456

    Open questions at the time
    • Cannot separate GFAP-specific from vimentin contributions
    • Molecular link between filament loss and Notch competence unresolved
  12. 2021 High

    Identified a specific reversible lipid modification of GFAP and its erasing enzyme, establishing palmitoylation as a driver of astrocyte proliferation, astrogliosis, and neurodegeneration.

    Evidence Palm-proteomics and in vitro palmitoylation assay; C291A site-directed mutagenesis; PPT1-knockin mouse with functional rescue and astrogliosis markers

    PMID:33753498

    Open questions at the time
    • Palmitoyltransferase that adds the modification not identified
    • Mechanistic link between palmitoylation and filament dynamics unresolved
  13. 2017 Medium

    Extended GFAP+ glial function to the periphery, showing GFAP+ satellite glia in sympathetic ganglia modulate cardiovascular output through neurotransmitter release.

    Evidence hM3Dq DREADD in GFAP+ cells with CNO activation, cardiovascular measurement, and beta-blocker dissection

    PMID:28138563

    Open questions at the time
    • Did not establish a direct role for GFAP protein itself versus the GFAP+ cell type
    • Mechanism of neurotransmitter release control unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the GFAP filament network mechanically and biochemically couples to organelle positioning, secretory function, and signaling competence—and how palmitoylation, isoform balance, and disease mutations converge on these outputs—remains unresolved.
  • No structural model linking filament organization to organelle/secretory defects
  • Palmitoyltransferase for GFAP unidentified
  • Causal hierarchy among aggregation, chaperone sequestration, JNK, and organelle dysfunction in Alexander disease not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 2 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2
Pathway
R-HSA-1643685 Disease 3 R-HSA-74160 Gene expression (Transcription) 2
Partners
CRYABHSPB1PLECPPT1VIM
Complex memberships
Rosenthal fibers

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1985 GFAP is the major protein constituent of glial intermediate filaments in differentiated fibrous and protoplasmic astrocytes of the CNS, functioning as a cytoskeletal component that defines and maintains the shape of astrocytes. Biochemical characterization, immunochemical and immunocytochemical studies Journal of neuroimmunology High 2409105
1985 Dibutyryl cyclic AMP (dbcAMP) increases GFAP synthesis in cultured astrocytes, as demonstrated by radioactive methionine labeling showing increased GFAP and vimentin synthesis within 48 h of exposure. Radioactive metabolic labeling of primary astrocyte cultures treated with dbcAMP Journal of neuroimmunology Medium 2989328
1989 Schwann cell expression of GFAP is developmentally regulated and requires continued trophic input from small axons; sciatic nerve transection causes marked reduction in GFAP mRNA in the distal stump, demonstrating axon-dependent regulation of GFAP in peripheral glia. Northern blot of sciatic nerve RNA after nerve transection; immunohistology of teased nerve fascicles Journal of neuroscience research Medium 2769798
1990 GFAP turnover in cultured astrocytes is biphasic, with a fast-decaying pool (half-life ~16–18 h) and a stable pool (half-life ~5–6 days); the stable pool increases proportionally as astrocytes mature, reflecting dynamic regulation of GFAP during differentiation. Pulse-chase radiolabeling of primary astroglial cultures at different developmental stages Brain research. Developmental brain research Medium 2279327
1991 Insulin-related peptides regulate GFAP expression and astrocyte morphology in organotypic cerebellar cultures; high insulin levels increase GFAP mRNA and protein with enrichment of radial glial morphology, while low insulin levels produce undifferentiated epithelioid cells with minimal GFAP expression. Organotypic cultures of E17 mouse cerebellum with varying insulin concentrations; non-isotopic in situ hybridization for GFAP mRNA; GFAP immunoreactivity Brain research Medium 1782546
1994 A 2.2 kb 5'-flanking sequence of the human GFAP gene is sufficient to direct astrocyte-specific expression in transgenic mice and recapitulates injury-induced upregulation of GFAP, demonstrating that key transcriptional regulatory elements reside in this promoter region. Transgenic mice carrying GFAP-promoter-lacZ reporter; histochemical staining after CNS injury The Journal of neuroscience High 8120611
1998 TGF-β1 significantly increases GFAP mRNA and protein in astrocytes, while FGF-2 significantly decreases GFAP mRNA and protein and inhibits TGF-β1-mediated increases; FGF-2 effects are blocked by an FGFR tyrosine kinase inhibitor, indicating receptor-mediated signaling. Primary astrocyte cultures treated with TGF-β1 and FGF-2; Western blot and mRNA analysis; pharmacological inhibition with 5'-methylthioadenosine and cycloheximide Glia Medium 9537840
1999 Neurons secrete brain-region-specific soluble factors that activate the GFAP gene promoter in astrocytes, inducing glial differentiation and cell cycle arrest, as demonstrated using transgenic astrocytes carrying a GFAP promoter-β-galactosidase reporter. Co-culture of neurons and transgenic astrocytes (GFAP-promoter-β-gal reporter mice); conditioned medium experiments; cell cycle analysis Glia Medium 10384875
2002 GFAP coding mutations in Alexander disease are heterozygous missense mutations found in the 1A, 2A, and 2B rod domains and the tail region; all are de novo dominant mutations, and the disease likely results from a dominant gain-of-function (partial block of filament assembly leading to accumulation of a toxic intermediate) rather than dominant loss-of-function, since GFAP null mice do not display Alexander disease symptoms. Sequencing of GFAP coding regions from Alexander disease patients; genetic analysis of multiple disease cases; comparison with GFAP null mouse phenotype International journal of developmental neuroscience High 12175861
2003 GFAP contains novel splice forms (Δ135 nt, Δexon 6, Δ164 nt) expressed as out-of-frame variants in neurons (pyramidal neurons of hippocampus), particularly associated with Alzheimer's disease pathology and Down syndrome, demonstrating cell-type-specific alternative splicing of GFAP. RT-PCR identification of novel splice variants; immunohistochemistry on human hippocampal tissue from AD, Down syndrome, and control cases Molecular psychiatry Medium 12931206
2005 The Alexander disease-causing R239C mutation in GFAP causes filament disorganization and decreased solubility: in SW13Vim(-) cells R239C GFAP forms diffuse/irregular rather than filamentous networks, and Triton-X-100 extraction shows R239C GFAP is more resistant to solubilization. Both wild-type and R239C GFAP assemble into 10 nm filaments in vitro with similar morphology, indicating the mutation affects network organization and solubility rather than filament formation per se. Transient transfection of R239C GFAP into SW13Vim(-) cells, primary rat astrocytes, Cos-7 cells; Triton-X-100 extraction; in vitro filament assembly assay Journal of cell science High 15840648
2005 LIF signaling generates GFAP+ cells that retain progenitor characteristics (remain in cell cycle, self-renew, enhanced neurogenesis), while BMP signaling generates GFAP+ cells that are stellate, exit cell cycle, and lack progenitor traits. In vivo, transgenic BMP4 overexpression increases GFAP+ astrocytes but depletes the GFAP+ progenitor pool, while BMP inhibition has the opposite effect. Treatment of cultured embryonic SVZ progenitors with LIF or BMP; transgenic mice overexpressing BMP4 or inhibitor of BMP signaling; cell cycle analysis; immunostaining Development High 16314487
2007 GFAP mutations in Alexander disease cause: (i) GFAP accumulation and Rosenthal fiber formation, (ii) sequestration of protein chaperones αB-crystallin and HSP27 into Rosenthal fibers, and (iii) activation of JNK and the stress response, collectively driving disease pathogenesis. Review synthesizing data from patient tissue, cell transfection studies, and mouse models; immunostaining for chaperones in Rosenthal fibers; JNK activation assays Experimental cell research Medium 17498694
2008 Glutamate activates the GFAP gene promoter in astrocytes through metabotropic glutamate receptors (mGluR2/3), triggering TGF-β1 secretion, which activates Smad transcription factor nuclear translocation; MAPK and PI3K pathways are also required for TGF-β1-induced GFAP gene activation, suggesting cooperation between canonical (Smad) and non-canonical TGF-β pathways. Transgenic astrocytes with GFAP-promoter-β-gal reporter; neutralizing antibodies against TGF-β; mGluR antagonist MCPG; MAPK inhibitor PD98059; PI3K inhibitor LY294002; Smad-2 phosphorylation assay Journal of neurochemistry Medium 18419760
2008 The human GFAP promoter contains specific DNA elements required for astrocyte specificity and region-specific expression: a 45 bp sequence (bp -1443 to -1399, C1.2) is required for silencing GFAP expression in neurons, and a 55 bp segment (bp -1488 to -1434, C1.1) contains region-specific elements. Transgenic mice carrying GFAP promoter deletion constructs linked to lacZ reporter; brain region analysis of reporter expression Glia Medium 18240313
2008 Mutant GFAP (Alexander disease), 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 stress resistance in primary astrocyte cultures. Primary astrocyte cultures from GFAP over-expressing transgenic mice and GFAP knock-in (R236H) mice; immunostaining; proteasome activity assays; cell proliferation and death assays; stress challenge Experimental cell research Medium 19146851
2011 SIN3A coupled with MeCP2 binds to the GFAP promoter to repress GFAP transcription; upon astrocyte differentiation, SIN3A-MeCP2 departs and activated STAT3 binds to the promoter and exon 1, recruiting CBP/p300 to exon 1, leading to H3K9 and H3K14 acetylation and H3K4 trimethylation that activate GFAP gene transcription. ChIP assays for SIN3A, MeCP2, STAT3, CBP/p300, RNA Pol II, histone marks; NTera-2 cell differentiation into astrocyte-like lineage PloS one High 21779366
2013 GFAP promoter activity is regulated by NFI, SP1, STAT3, and NF-κB binding sites (but not the consensus AP-1 site) within the B region (bp -1612 to -1489), with each subregion contributing cooperatively to transcriptional strength and astrocyte specificity. Transgenic mice with block mutations and specific transcription factor binding site mutations in GFAP promoter-reporter constructs; analysis of expression level, brain region pattern, and astrocyte specificity Glia Medium 23832770
2013 MeCP2 binds to methylated regions of the GFAP promoter and represses GFAP expression; siRNA knockdown of MeCP2 in the developing female rat amygdala and hypothalamus specifically increases GFAP mRNA and protein without altering other astrocyte markers (S100β, vimentin). MeCP2 siRNA infusion into rat brain; RT-PCR and Western blot for GFAP, S100β, and vimentin; sex-specific analysis Brain research Medium 24269336
2014 HDAC inhibition (trichostatin A or sodium butyrate) reduces GFAP expression in human astrocytes and astrocytoma cells and increases the GFAPδ:GFAPα ratio, with the alternative isoform expression being dependent on SR protein splicing factors. HDAC inhibition also induces aggregation of the GFAP network resembling Alexander disease pathology. Primary human astrocytes and astrocytoma cells treated with HDAC inhibitors; qRT-PCR for isoforms; immunostaining for network organization; siRNA knockdown of SR proteins Journal of cell science Medium 25128567
2014 Shifting the GFAP isoform ratio toward GFAPδ (by shRNA silencing of GFAPα) decreases plectin expression and increases laminin expression, resulting in decreased astrocytoma cell motility. Pan-GFAP silencing leads to decreased cell spreading, increased integrin expression, and >100-fold increase in cell adhesion to laminin, demonstrating isoform-specific roles of GFAP in regulating extracellular matrix interactions. Isoform-specific shRNA silencing of GFAPα in astrocytoma cells; migration/motility assays; integrin and laminin expression analysis; cell adhesion assay FASEB journal Medium 24696300
2016 GFAPδ exchanges more slowly with the intermediate filament network than GFAPα as measured by FRAP; GFAPδ-induced IF network collapse further decreases exchange rates of both isoforms and alters cell morphology and focal adhesion size without affecting cell migration or proliferation. FRAP of fluorescently tagged GFAPα and GFAPδ in astrocytoma cells; immunostaining for focal adhesions; migration and proliferation assays Cellular and molecular life sciences Medium 27141937
2017 Gq-GPCR activation specifically in peripheral GFAP+ satellite glial cells (within sympathetic ganglia) leads to increased norepinephrine release, beta-1 adrenergic receptor activation in the heart, and consequent acceleration of heart rate and increased left ventricular contraction, demonstrating a functional role for GFAP+ glia in regulating cardiovascular function. Transgenic mice expressing hM3Dq DREADD in GFAP+ cells; pharmacological activation with clozapine N-oxide; cardiovascular measurements; beta-blocker pharmacological dissection JCI insight Medium 28138563
2018 AxD-causing GFAP mutations in iPSC-derived human astrocytes cause GFAP aggregates, enlarged and perinuclearly localized endoplasmic reticulum and lysosomes, impaired extracellular ATP release, and attenuated calcium wave propagation, revealing that mutant GFAP disrupts intracellular vesicle regulation and astrocyte secretory function. iPSC-derived astrocytes from AxD patients with isogenic correction; RNA-seq; organelle morphology imaging; ATP release assay; calcium imaging Cell reports High 30355500
2019 GFAP and vimentin deficiency (GFAP-/-Vim-/- mice) results in decreased Notch signal-sending competence in astrocytes and altered expression of Notch signaling pathway genes (Dlk2, Notch1, Sox2), demonstrating that astrocyte intermediate filaments regulate Notch signaling capacity. Single-cell RT-qPCR on freshly isolated astrocytes from GFAP-/-Vim-/- and wild-type mice; hippocampal entorhinal cortex lesion model Journal of neurochemistry Medium 26118771
2021 GFAP is palmitoylated in vitro and in vivo at a unique site, cysteine-291; PPT1 is the depalmitoylating enzyme for GFAP; palmitoylated GFAP promotes astrocyte proliferation in vitro; in PPT1-knockin mice, hyperpalmitoylated GFAP drives astrogliosis and neurodegeneration, and mutating C291A attenuates astrogliosis and concurrent neurodegeneration. Palm-proteomics; in vitro palmitoylation assay; site-directed mutagenesis (C291A); PPT1-KI mouse model; astrocyte proliferation assays; immunohistology for astrogliosis markers Proceedings of the National Academy of Sciences of the United States of America High 33753498
2019 GFAP and vimentin double-knockout (GFAP-/-Vim-/-) mice show more pronounced memory extinction compared to wildtype mice in IntelliCage reversal learning, while other learning and memory measures are comparable, indicating a specific role for astrocyte intermediate filaments in hippocampal circuit reorganization. GFAP-/-Vim-/- mice; open field, object recognition, Morris water maze, trace fear conditioning, IntelliCage reversal learning behavioral tests Biological chemistry Medium 31063456

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 GFAP in health and disease. Progress in neurobiology 849 21219963
1994 GFAP and astrogliosis. Brain pathology (Zurich, Switzerland) 738 7952264
2015 Glial fibrillary acidic protein (GFAP) and the astrocyte intermediate filament system in diseases of the central nervous system. Current opinion in cell biology 699 25726916
1985 Glial fibrillary acidic protein (GFAP): the major protein of glial intermediate filaments in differentiated astrocytes. Journal of neuroimmunology 675 2409105
1994 GFAP promoter directs astrocyte-specific expression in transgenic mice. The Journal of neuroscience : the official journal of the Society for Neuroscience 430 8120611
1993 GFAP mRNA increases with age in rat and human brain. Neurobiology of aging 348 8247224
2008 GFAP promoter elements required for region-specific and astrocyte-specific expression. Glia 321 18240313
2006 GFAP transgenic zebrafish. Gene expression patterns : GEP 302 16765104
2005 LIF and BMP signaling generate separate and discrete types of GFAP-expressing cells. Development (Cambridge, England) 223 16314487
2021 Beyond the GFAP-Astrocyte Protein Markers in the Brain. Biomolecules 222 34572572
2011 GFAP mutations, age at onset, and clinical subtypes in Alexander disease. Neurology 204 21917775
2007 GFAP and its role in Alexander disease. Experimental cell research 156 17498694
2014 Enteric GFAP expression and phosphorylation in Parkinson's disease. Journal of neurochemistry 152 24749759
1999 Glial fibrillary acidic protein (GFAP): modulation by growth factors and its implication in astrocyte differentiation. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 152 10412574
1994 Structure and transcriptional regulation of the GFAP gene. Brain pathology (Zurich, Switzerland) 138 7952266
2003 Neuronal expression of GFAP in patients with Alzheimer pathology and identification of novel GFAP splice forms. Molecular psychiatry 133 12931206
2019 Clinical characteristics of autoimmune GFAP astrocytopathy. Journal of neuroimmunology 132 30991306
2003 Differential expression of GFAP in early v late AMD: a quantitative analysis. The British journal of ophthalmology 132 12928288
2017 Type III Intermediate Filaments Desmin, Glial Fibrillary Acidic Protein (GFAP), Vimentin, and Peripherin. Cold Spring Harbor perspectives in biology 111 29196434
2022 Blocking C3d+/GFAP+ A1 Astrocyte Conversion with Semaglutide Attenuates Blood-Brain Barrier Disruption in Mice after Ischemic Stroke. Aging and disease 107 35656116
2022 Association of plasma glial fibrillary acidic protein (GFAP) with neuroimaging of Alzheimer's disease and vascular pathology. Alzheimer's & dementia (Amsterdam, Netherlands) 106 35252538
2002 GFAP mutations in Alexander disease. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 106 12175861
2004 Expression specificity of GFAP transgenes. Neurochemical research 101 15662842
2021 Regulation of GFAP Expression. ASN neuro 100 33601918
2021 Glial Fibrillary Acidic Protein (GFAP): Neuroinflammation Biomarker in Acute Ischemic Stroke. Journal of inflammation research 99 35002283
2020 GFAP at 50. ASN neuro 96 32811163
2016 Assessment of Serum UCH-L1 and GFAP in Acute Stroke Patients. Scientific reports 92 27074724
2004 Non-invasive imaging of GFAP expression after neuronal damage in mice. Neuroscience letters 91 15331155
1998 Regulation of astrocyte GFAP expression by TGF-beta1 and FGF-2. Glia 91 9537840
2020 Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration. Journal of Alzheimer's disease : JAD 88 32804092
2017 GFAP expression in injured astrocytes in rats. Experimental and therapeutic medicine 88 28962102
1985 Regulation of glial fibrillary acidic protein (GFAP) expression in CNS development and in pathological states. Journal of neuroimmunology 86 2989328
1988 Ependymal and choroid plexus tumors. Cytokeratin and GFAP expression. Cancer 80 2449946
2022 Neuroinflammation Is Associated with GFAP and sTREM2 Levels in Multiple Sclerosis. Biomolecules 74 35204724
2003 GFAP: functional implications gleaned from studies of genetically engineered mice. Glia 73 12761871
1998 Correlation of B-FABP and GFAP expression in malignant glioma. Oncogene 73 9591779
1984 Glial fibrillary acidic protein (GFAP) immunoreactivity in peripheral nerve sheath tumors. Ultrastructural pathology 70 6543600
2019 Importance of GFAP isoform-specific analyses in astrocytoma. Glia 68 30667110
2005 Alexander-disease mutation of GFAP causes filament disorganization and decreased solubility of GFAP. Journal of cell science 66 15840648
2019 Enteric Glia: S100, GFAP, and Beyond. Anatomical record (Hoboken, N.J. : 2007) 65 30951262
1999 Neurons induce GFAP gene promoter of cultured astrocytes from transgenic mice. Glia 63 10384875
1996 GFAP Transgenic Mice. Methods (San Diego, Calif.) 61 8954847
1991 Developmental expression of the glial fibrillary acidic protein (GFAP) gene in the mouse retina. Cellular and molecular neurobiology 61 1723659
1996 Repeated seizures increase GFAP and vimentin in the hippocampus. Brain research 60 8738264
2010 Purity, cell viability, expression of GFAP and bystin in astrocytes cultured by different procedures. Journal of cellular biochemistry 58 19899109
2017 GFAP in early multiple sclerosis: A biomarker for inflammation. Neuroscience letters 57 28802830
2006 Astrocyte heterogeneity revealed by expression of a GFAP-LacZ transgene. Glia 57 16482522
2005 Olig2 expression, GFAP, p53 and 1p loss analysis contribute to glioma subclassification. Neuropathology and applied neurobiology 57 15634232
2024 Prediction of clinical progression in nervous system diseases: plasma glial fibrillary acidic protein (GFAP). European journal of medical research 55 38216970
2019 The role of GFAP and vimentin in learning and memory. Biological chemistry 55 31063456
2018 Mutations in GFAP Disrupt the Distribution and Function of Organelles in Human Astrocytes. Cell reports 55 30355500
2014 Histone acetylation in astrocytes suppresses GFAP and stimulates a reorganization of the intermediate filament network. Journal of cell science 54 25128567
2008 Glutamate activates GFAP gene promoter from cultured astrocytes through TGF-beta1 pathways. Journal of neurochemistry 54 18419760
1989 Neuronal modulation of Schwann cell glial fibrillary acidic protein (GFAP). Journal of neuroscience research 54 2769798
2021 Increased GFAP concentrations in the cerebrospinal fluid of patients with unipolar depression. Translational psychiatry 53 34021122
2011 Interplay between SIN3A and STAT3 mediates chromatin conformational changes and GFAP expression during cellular differentiation. PloS one 50 21779366
2005 Expression of MBP, PLP, MAG, CNP, and GFAP in the Human Alcoholic Brain. Alcoholism, clinical and experimental research 50 16205370
2003 GFAP promoter drives Müller cell-specific expression in transgenic mice. Investigative ophthalmology & visual science 50 12882814
1991 Insulin influences astroglial morphology and glial fibrillary acidic protein (GFAP) expression in organotypic cultures. Brain research 50 1782546
2021 GFAP hyperpalmitoylation exacerbates astrogliosis and neurodegenerative pathology in PPT1-deficient mice. Proceedings of the National Academy of Sciences of the United States of America 47 33753498
2010 Vimentin and GFAP responses in astrocytes after contusion trauma to the murine brain. Restorative neurology and neuroscience 47 20479526
2016 GFAP isoforms control intermediate filament network dynamics, cell morphology, and focal adhesions. Cellular and molecular life sciences : CMLS 44 27141937
1990 Müller cell GFAP expression exhibits gradient from focus of photoreceptor light damage. Current eye research 44 2200639
2021 GFAP positivity in neurons following traumatic brain injuries. International journal of legal medicine 43 34114049
2007 Glial fibrillary acidic protein (GFAP) and anti-GFAP autoantibody in canine necrotising meningoencephalitis. The Veterinary record 43 17720962
2008 Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice. Experimental cell research 42 19146851
1994 Normal and pathological expression of GFAP promoter elements in transgenic mice. Glia 40 7890332
1985 GFAP in brain tumor diagnosis: possibilities and limitations. Pathology, research and practice 40 4034433
2010 Drug screening to identify suppressors of GFAP expression. Human molecular genetics 39 20538881
2023 Hippocampal GFAP-positive astrocyte responses to amyloid and tau pathologies. Brain, behavior, and immunity 37 36878332
2017 Ganglionic GFAP glial Gq-GPCR signaling enhances heart functions in vivo. JCI insight 37 28138563
2013 Transgenic analysis of GFAP promoter elements. Glia 37 23832770
1990 GFAP turnover during astroglial proliferation and differentiation. Brain research. Developmental brain research 37 2279327
2015 CSF and Blood Levels of GFAP in Alexander Disease. eNeuro 36 26478912
2015 Heterogeneity of Notch signaling in astrocytes and the effects of GFAP and vimentin deficiency. Journal of neurochemistry 35 26118771
2013 MeCP2 regulates GFAP expression within the developing brain. Brain research 33 24269336
2022 Serum GFAP - reference interval and preanalytical properties in Danish adults. Clinical chemistry and laboratory medicine 32 36067832
2020 Plasma NfL and GFAP as biomarkers of spinal cord degeneration in adrenoleukodystrophy. Annals of clinical and translational neurology 32 33047897
2024 The GFAP proteoform puzzle: How to advance GFAP as a fluid biomarker in neurological diseases. Journal of neurochemistry 31 39289040
2014 Silencing GFAP isoforms in astrocytoma cells disturbs laminin-dependent motility and cell adhesion. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 31 24696300
2020 CSF levels of glutamine synthetase and GFAP to explore astrocytic damage in seronegative NMOSD. Journal of neurology, neurosurgery, and psychiatry 30 32217788
2002 GFAP expression withdraws--a trend of glial evolution? Brain research bulletin 30 11923020
1986 Anaplasia and heterogeneity of GFAP expression in gliomas. Tumori 30 3705189
2014 Immunohistochemical analysis of GFAP-δ and nestin in cerebral astrocytomas. Brain tumor pathology 29 25178519
2012 Serum GFAP levels in optic neuropathies. Journal of the neurological sciences 29 22410258
2023 Plasma GFAP associates with secondary Alzheimer's pathology in Lewy body disease. Annals of clinical and translational neurology 28 37000892
2021 Expression of GFAP and Tau Following Blast Exposure in the Cerebral Cortex of Ferrets. Journal of neuropathology and experimental neurology 28 33421075
2012 Quantitative analysis of GFAP- and S100 protein-immunopositive astrocytes to investigate the severity of traumatic brain injury. Legal medicine (Tokyo, Japan) 28 22301378
2022 GFAP Alternative Splicing and the Relevance for Disease - A Focus on Diffuse Gliomas. ASN neuro 27 35673702
2015 Striatal Injury with 6-OHDA Transiently Increases Cerebrospinal GFAP and S100B. Neural plasticity 26 26090233
1991 Schwann cell GFAP expression increases in axonal neuropathies. Journal of the neurological sciences 26 1649261
2016 Anorexia Reduces GFAP+ Cell Density in the Rat Hippocampus. Neural plasticity 25 27579183
2024 GFAP-isoforms in the nervous system: Understanding the need for diversity. Current opinion in cell biology 24 38401182
2013 GFAP expression and social deficits in transgenic mice overexpressing human sAPPα. Glia 24 23840007
2011 Archetypal and new families with Alexander disease and novel mutations in GFAP. Archives of neurology 24 21987397
1992 Glial fibrillary acidic protein (GFAP) expression and nucleolar organizer regions (NORs) in human gliomas. Brain research 24 1319273
2019 Refining the concept of GFAP toxicity in Alexander disease. Journal of neurodevelopmental disorders 23 31838996
2016 Asymmetric Distribution of GFAP in Glioma Multipotent Cells. PloS one 23 26953813
2024 Serum NfL and GFAP as biomarkers of progressive neurodegeneration in TBI. Alzheimer's & dementia : the journal of the Alzheimer's Association 21 38805359
2023 Striatal spatial heterogeneity, clustering, and white matter association of GFAP+ astrocytes in a mouse model of Huntington's disease. Frontiers in cellular neuroscience 21 37187609

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