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GFAP encodes one of the major intermediate filament proteins of mature astrocytes. Additionally we are shipping GFAP Antibodies (815) and GFAP Kits (54) 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.
GFAP is upregulated following an insult or injury to the brain, additionally making it an indicator of CNS pathology.
This study demonistrated that the density of GFAP-immunoreactive astrocytes is decreased in left hippocampi in major depressive disorder
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.
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.
This study demonstrated the GFAP-ApoE4 mice exhibited motor impairments when compared to GFAP-ApoE3 and wild-type mice.
PINK1 (show PINK1 Proteins) deficiency causes defects in GFAP-positive astrogliogenesis during brain development.
Gnasxl (show GNAS Proteins) deficiency does not directly affect glial development in the hypothalamus, since it is expressed in neurons, and Gfap-positive astrocytes and tanycytes appear normal during early postnatal stages.
Induction of glial cytokine expression was sequential, aligned with active sickness behavior, and preceded increased Iba-1 (show AIF1 Proteins) or GFAP immunoreactivity after lipopolysaccharide challenge
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
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