ArticleMolecular biology of the cell2008
Glial fibrillary acidic protein filaments can tolerate the incorporation of assembly-compromised GFAP-delta, but with consequences for filament organization and alphaB-crystallin association.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 106 citations in OpenAlex.
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- Catch-and-Display Immunoassay as an Accessible Platform for Digital Biomarker Detection.bioRxiv : the preprint server for biology · 2026Article
- Linking Cell Architecture to Mitochondrial Signaling in Neurodegeneration: The Role of Intermediate Filaments.International journal of molecular sciences · 2025Review
- The Role of Glial Fibrillary Acidic Protein in the Neuropathology of Alzheimer's Disease and Its Potential as a Blood Biomarker for Early Diagnosis and Progression.Molecular neurobiology · 2025Review
- GFAPβ and GFAPδ Isoforms Expression in Mesenchymal Stem Cells, MSCs Differentiated Towards Schwann-like, and Olfactory Ensheathing Cells.Current issues in molecular biology · 2025Article
- The GFAP proteoform puzzle: How to advance GFAP as a fluid biomarker in neurological diseases.Journal of neurochemistry · 2025Review
- Effects of Alexander disease-associated mutations on the assembly and organization of GFAP intermediate filaments.Molecular biology of the cell · 2022Article
- GFAP splice variants fine-tune glioma cell invasion and tumour dynamics by modulating migration persistence.Scientific reports · 2022Article
- GFAPδ: A Promising Biomarker and Therapeutic Target in Glioblastoma.Frontiers in oncology · 2022Review
- Glial Fibrillary Acidic Protein in Blood as a Disease Biomarker of Neuromyelitis Optica Spectrum Disorders.Frontiers in neurology · 2022Review
- Susceptibility of cytoskeletal-associated proteins for tumor progression.Cellular and molecular life sciences : CMLS · 2021Review
- New GFAP splice isoform (GFAPµ) differentially expressed in glioma translates into 21 kDa N-terminal GFAP protein.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Astrocyte phenotypes: Emphasis on potential markers in neuroinflammation.Histology and histopathology · 2021Review
- Review
- Type II Alexander disease caused by splicing errors and aberrant overexpression of an uncharacterized GFAP isoform.Human mutation · 2020Article
- Astrocyte-Oligodendrocyte-Microglia Crosstalk in Astrocytopathies.Frontiers in cellular neuroscience · 2020Review
- Filaments and phenotypes: cellular roles and orphan effects associated with mutations in cytoplasmic intermediate filament proteins.F1000Research · 2019Review
- Antisense suppression of glial fibrillary acidic protein as a treatment for Alexander disease.Annals of neurology · 2018Article
- Type III Intermediate Filaments Desmin, Glial Fibrillary Acidic Protein (GFAP), Vimentin, and Peripherin.Cold Spring Harbor perspectives in biology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The glial fibrillary acidic protein (GFAP) gene is alternatively spliced to give GFAP-alpha, the most abundant isoform, and seven other differentially expressed transcripts including GFAP-delta. GFAP-delta has an altered C-terminal domain that renders it incapable of self-assembly in vitro. When titrated with GFAP-alpha, assembly was restored providing GFAP-delta levels were kept low (approximately 10%). In a range of immortalized and transformed astrocyte derived cell lines and human spinal cord, we show that GFAP-delta is naturally part of the endogenous intermediate filaments, although levels were low (approximately 10%). This suggests that GFAP filaments can naturally accommodate a small proportion of assembly-compromised partners. Indeed, two other assembly-compromised GFAP constructs, namely enhanced green fluorescent protein (eGFP)-tagged GFAP and the Alexander disease-causing GFAP mutant, R416W GFAP both showed similar in vitro assembly characteristics to GFAP-delta and could also be incorporated into endogenous filament networks in transfected cells, providing expression levels were kept low. Another common feature was the increased association of alphaB-crystallin with the intermediate filament fraction of transfected cells. These studies suggest that the major physiological role of the assembly-compromised GFAP-delta splice variant is as a modulator of the GFAP filament surface, effecting changes in both protein- and filament-filament associations as well as Jnk phosphorylation.
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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.