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GFAP encodes one of the major intermediate filament proteins of mature astrocytes.
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Rat (Rattus) GFAP ELISA Kit für Sandwich ELISA - ABIN416142
Tskitishvili, Nisolle, Munaut, Pequeux, Gerard, Noel, Foidart: Estetrol attenuates neonatal hypoxic-ischemic brain injury. in Experimental neurology 2014
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Human GFAP ELISA Kit für Sandwich ELISA - ABIN365729
Akdemir, Yardan, Kati, Duran, Alacam, Yavuz, Okuyucu: The role of S100B protein, neuron-specific enolase, and glial fibrillary acidic protein in the evaluation of hypoxic brain injury in acute carbon monoxide poisoning. in Human & experimental toxicology 2014
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Human GFAP ELISA Kit für Sandwich ELISA - ABIN414459
Ekingen, Yilmaz, Yildiz, Atescelik, Goktekin, Gurger, Alatas, Basturk, Ilhan: Utilization of glial fibrillary acidic protein and galectin-3 in the diagnosis of cerebral infarction patients with normal cranial tomography. in Nigerian journal of clinical practice 2017
Rat (Rattus) GFAP ELISA Kit für Sandwich ELISA - ABIN367441
Moallem, Mohamadpour, Abnous, Sankian, Sadeghnia, Tsatsakis, Shahsavand: Erythropoietin in the treatment of carbon monoxide neurotoxicity in rat. in Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 2015
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 Concentrations of microparticles expressing GFAP and AQP4 (zeige AQP4 ELISA Kits) were significantly higher in the traumatic brain injury group compared with healthy controls.
The authors observed higher serum levels of GFAP and UCH-L1 (zeige UCHL1 ELISA Kits) in brain-injured children compared with controls and also demonstrated a step-wise increase of biomarker concentrations over the continuum of severity from mild to severe traumatic brain injury. Serum UCH-L1 (zeige UCHL1 ELISA Kits) and GFAP concentrations also strongly predicted poor outcome.
Study examined if QKI6B expression can predict the outcome of GFAP, and several oligodendrocyte-related genes, in the prefrontal cortex of brain samples of schizophrenic individuals. QKI6B significantly predicts the expression of GFAP, but does not predict oligodendrocyte-related gene outcome, as previously seen with other QKI isoforms.
GFAP, along with tau and AmyloidBeta42, were increased in plasma up to 90 days after traumatic brain injury compared with controls.
Results show that the positive rates and expression levels of nestin (zeige NES ELISA Kits), tyrosine hydroxylase (TH (zeige TH ELISA Kits)), GFAP and IL-17 (zeige IL17A ELISA Kits) were significantly decreased while Foxp3 (zeige FOXP3 ELISA Kits) and the ratio of Foxp3 (zeige FOXP3 ELISA Kits)/IL-17 (zeige IL17A ELISA Kits) were statistically elevated in BM of AML (zeige RUNX1 ELISA Kits) patients.
GFAP levels >0.29 ng/ml were seen only in intracerebral hemorrhage, thus confirming the diagnosis of ICH (zeige COL4a2 ELISA Kits) during prehospital care.
These results indicate that autoantibodies against GFAP could serve as a predictive marker for the development of overt autoimmune diabetes.
Higher median plasma GFAP values were documented in intracerebral hemorrhage compared with acute ischemic stroke, stroke mimics, and controls.
GFAP is specifically expressed in the auricular chondrocytes, and assumes a pivotal role in resistance against mechanical stress.
Bevacizumab treatment was also associated with structural protein abnormalities, with decreased GFAP and vimentin (zeige VIM ELISA Kits) content and upregulated GFAP and vimentin (zeige VIM ELISA Kits) mRNA expression.
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 report the successful prediction and validation of Gfap as an miR (zeige MLXIP ELISA Kits)-3099 target gene using a combination of bioinformatics resources with enrichment of annotations based on functional ontologies and a spatio-temporal expression dataset.
compared open-skull and thinned-skull imaging methods for two-photon laser microscopy of live astrocytes in neocortex of GFAP-GFP transgenic mice
work reveals that an Alexander disease-causing mutation alters GFAP turnover kinetics in vivo and provides an essential foundation for future studies aimed at preventing or reducing the accumulation of GFAP.
Tat (zeige TAT ELISA Kits) expression or GFAP expression led to formation of GFAP aggregates and induction of unfolded protein response (UPR) and endoplasmic reticulum (ER) stress in astrocytes.
Study provides evidence that transcription of one of the astrocyte-specific genes, Gfap, is cooperatively regulated by co-expressed genes and their regulatory factors.
This study demonstrated the GFAP-ApoE4 mice exhibited motor impairments when compared to GFAP-ApoE3 and wild-type mice.
PINK1 deficiency causes defects in GFAP-positive astrogliogenesis during brain development.
Gnasxl (zeige GNAS ELISA Kits) 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.
Aggregation-prone GFAP mutation in Alexander disease was validated using a zebrafish model; The p.Asp128Asn GFAP mutation is likely to be a disease-causing mutation
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 (zeige SOX2 ELISA Kits), 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