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GFAP encodes one of the major intermediate filament proteins of mature astrocytes. Additionally we are shipping GFAP Antibodies (707) and GFAP Kits (63) and many more products for this protein.
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There was significantly more GFAP immunoreactivity in the prefrontal cortex and hippocampus of aged animals compared to adult or middle-aged animals.
This study demonstrated that GFAP as a promising biomarker to distinguish ischemic stroke from intracerebral hemorrhage.
The levels of GFAP in Alzheimer's disease, dementia with Lewy bodies, and frontotemporal lobar degeneration patients were significantly higher than those in the healthy control subjects.
GFAP is significantly associated with outcome, but it does not add predictive power to commonly used prognostic variables in a population of patients with TBI (show TBPL1 Proteins) of varying severities.
Neither duplications nor deletions of GFAP were found, suggesting that GFAP coding-region rearrangements may not be involved in Alexander disease or Alexanderrelated leukoencephalopathies.
The data suggest that human vitreous body GFAP is a protein biomarker for glial activation in response to retinal pathologies.
Studied diagnostic Value of Serum Levels of GFAP, pNF-H, and NSE (show ENO2 Proteins) Compared With Clinical Findings in Severity Assessment of Human Traumatic Spinal Cord Injury.
GFAP peaks early during haemorrhagic brain lesions (at significantly higher levels), and late in ischaemic events, whereas antibodies against NR2 RNMDA have significantly higher levels during ischemic stroke at all time-points.
There was an absence of GFAP in astrocytes during early fetal spinal cord development until 9 months of gestation , and the appearance of GFAP-positive reactivity was later than that of neurons.
These data imply that a tight regulation of histone acetylation in astrocytes is essential, because dysregulation of gene expression causes the aggregation of GFAP, a hallmark of human diseases like Alexander's disease.
Identification of a novel nonsense mutation in the rod domain of GFAP that is associated with Alexander disease.
Isolation of an evolutionary conserved novel GFAP isoform, GFAPkappa, produced by alternative splicing and polyadenylation of the 3'-region of the human GFAP pre-mRNA is described.
Study provides a mechanistic link between the GFAP mutations/overexpression and the symptoms in those affected with Type II Alexander disease
Study described GFAP-expressing non-myelinating Schwann cells in the lung, validated a transgenic mouse line that drives expression of cre under a GFAP promoter
findings thus show that the inability to produce GFAP and Vim (show VIM Proteins) affects normal retinal physiology and that the effect of IF deficiency on retinal cell survival differs, depending on the underlying pathologic condition
CUL4B (show CUL4B Proteins) as a negative regulator of GFAP expression during neural development.
Astrocytes deficient of GFAP and vimentin (show VIM Proteins) showed decreased Notch (show NOTCH1 Proteins) signal sending competence and altered expression of Notch (show NOTCH1 Proteins) signaling pathway-related genes
Absence of GFAP, or both GFAP and vimentin (show VIM Proteins), alters Alzheimer's disease-induced changes in gene expression profile of astrocytes, showing a compensation of the decrease of neuronal support genes and a trend for a higher inflammatory expression profile
immunohistochemistry revealed increased numbers of GFAP/BDNF (show BDNF Proteins) double-positive cells, which agrees with the observed changes in the culture system
Data indicate that glial fibrillary acidic protein (GFAP) was up-regulated in satellite glial cells (SGCs) in dorsal root ganglia 14 days after streptozotocin injection.
Findings demonstrate that ENT1 (show SLC29A1 Proteins) regulates GFAP expression and possibly astrocyte function
Data suggest that prenatal alterations in expression of various fetal brain proteins (including down-regulation of Gfap) are associated with aberrant behavioral characteristics of transgenic mice that model autism-like behavior.
The distribution of GFAP immunoreactivity implies that enteric glia are widespread in the fish gastrointestinal tract.
Generation of transgenic zebrafish that express green fluorescent protein (GFP) in glial cells driven by the zebrafish glial fibrillary acidic protein (GFAP) regulatory elements.
Cells expressing the two reporters display radial glial morphology, colocalize with the NSC marker Sox2 (show SOX2 Proteins), undergo proliferation, and are capable of self-renewal within the matrix of distinct thickness in the telencephalon.
This gene encodes one of the major intermediate filament proteins of mature astrocytes. It is used as a marker to distinguish astrocytes from other glial cells during development. Mutations in this gene cause Alexander disease, a rare disorder of astrocytes in the central nervous system. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
glial fibrillary acidic protein
, glial fibrillary acidic protein alpha
, intermediate filament
, intermediate filament protein
, zrf-1 antigen