Glial Fibrillary Acidic Protein (GFAP) ELISA试剂盒

Rhesus Monkey Glial Fibrillary Acidic Protein (GFAP) interaction partners

1. There was significantly more GFAP immunoreactivity in the prefrontal cortex and hippocampus of aged animals compared to adult or middle-aged animals.

Human Glial Fibrillary Acidic Protein (GFAP) interaction partners

1. serum levels do not increase in diabetic ketoacidosis patients without overt brain injury

2. Post-mortem GFAP serum concentrations correlate with agony time and might therefore be useful for the evaluation of the severity of brain damage in prolonged death. Elevated GFAP serum levels do not indicate a primary cerebral cause of death.

3. Spearman's rank correlation analysis and Bonferroni correction were used to compare the values of DKI and the expression levels of GFAP, Topo IIalpha, and MGMT between the 2 groups.

4. The obtained data testify higher specificity and sensitivity of glio-fibrillar acid protein as a biochemical marker of glioblastoma appropriate to be applied in case of primary examination of patients with brain affection.

5. serum level not significantly elevated in newborns at risk for hypoxic ischemic encephalopathy but with normal EEGs

6. crystal structure of human GFAP spanning the central coiled-coil 1B domain at 2.5A resolution

7. GFAP levels are a novel and complementary biomarker to predict functional outcome 1 year after acute ischemic stroke.

8. The features of the neuropathology and immunopathology of GFAP astrocytopathies were perivascular inflammation and loss of astrocytes and neurons

9. amniotic fluid -GFAP levels differentiate between myelomeningocele and myeloschisis, and raise interesting questions regarding the clinical significance between the 2 types of defects.

10. Desmin, Glial Fibrillary Acidic Protein, Vimentin, and Peripherin are type III intermediate filaments that have roles in health and disease [review]

11. Plasma concentration of GFAP demonstrated associations with stroke occurrence in a West African cohort but was not associated with stroke severity or mortality.

12. This study demonstrated that Concentrations of microparticles expressing GFAP and AQP4 were significantly higher in the traumatic brain injury group compared with healthy controls.

13. The authors observed higher serum levels of GFAP and UCH-L1 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 and GFAP concentrations also strongly predicted poor outcome.

14. 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.

15. GFAP, along with tau and AmyloidBeta42, were increased in plasma up to 90 days after traumatic brain injury compared with controls.

16. Results show that the positive rates and expression levels of nestin, tyrosine hydroxylase (TH), GFAP and IL-17 were significantly decreased while Foxp3 and the ratio of Foxp3/IL-17 were statistically elevated in BM of AML patients.

17. GFAP levels >0.29 ng/ml were seen only in intracerebral hemorrhage, thus confirming the diagnosis of ICH during prehospital care.

18. These results indicate that autoantibodies against GFAP could serve as a predictive marker for the development of overt autoimmune diabetes.

19. Higher median plasma GFAP values were documented in intracerebral hemorrhage compared with acute ischemic stroke, stroke mimics, and controls.

20. GFAP is specifically expressed in the auricular chondrocytes, and assumes a pivotal role in resistance against mechanical stress.

Pig (Porcine) Glial Fibrillary Acidic Protein (GFAP) interaction partners

1. 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.

Mouse (Murine) Glial Fibrillary Acidic Protein (GFAP) interaction partners

1. Study demonstrated that protein citrullination, along with upregulation and an increase in peptidylarginine deiminase, occur in a widely used bile duct ligation (BDL) mouse model of hepatic fibrosis. Expression level of GFAP and the amount of cit-GFAP were higher in BDL livers than in control livers. In correlation with PAD2 localization, cit-GFAP was observed in alpha-SMA-positive and CK19-positive cells in the livers.

2. The results indicate that finely tuned levels of Lmnb1 are required for neural stem cells differentiation into neurons, proper expression of the astrocytic marker GFAP and corticogenesis.

3. The results suggest that BRG1 and STAT3 coordinately regulate gene clustering and up-regulate Gfap and Osmr transcription in astrocytes.

4. This report the successful prediction and validation of Gfap as an miR-3099 target gene using a combination of bioinformatics resources with enrichment of annotations based on functional ontologies and a spatio-temporal expression dataset.

5. These results indicate that autoantibodies against GFAP could serve as a predictive marker for the development of overt autoimmune diabetes.

6. GFAP is specifically expressed in the auricular chondrocytes, and assumes a pivotal role in resistance against mechanical stress.

7. compared open-skull and thinned-skull imaging methods for two-photon laser microscopy of live astrocytes in neocortex of GFAP-GFP transgenic mice

8. 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.

9. Tat expression or GFAP expression led to formation of GFAP aggregates and induction of unfolded protein response (UPR) and endoplasmic reticulum (ER) stress in astrocytes.

10. Study provides evidence that transcription of one of the astrocyte-specific genes, Gfap, is cooperatively regulated by co-expressed genes and their regulatory factors.

11. This study demonstrated the GFAP-ApoE4 mice exhibited motor impairments when compared to GFAP-ApoE3 and wild-type mice.

12. PINK1 deficiency causes defects in GFAP-positive astrogliogenesis during brain development.

13. Gnasxl 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.

14. Induction of glial cytokine expression was sequential, aligned with active sickness behavior, and preceded increased Iba-1 or GFAP immunoreactivity after lipopolysaccharide challenge

15. Study provides a mechanistic link between the GFAP mutations/overexpression and the symptoms in those affected with Type II Alexander disease

16. 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

17. findings thus show that the inability to produce GFAP and Vim affects normal retinal physiology and that the effect of IF deficiency on retinal cell survival differs, depending on the underlying pathologic condition

18. CUL4B as a negative regulator of GFAP expression during neural development.

19. Astrocytes deficient of GFAP and vimentin showed decreased Notch signal sending competence and altered expression of Notch signaling pathway-related genes

20. Absence of GFAP, or both GFAP and vimentin, 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

Zebrafish Glial Fibrillary Acidic Protein (GFAP) interaction partners

1. 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

2. The distribution of GFAP immunoreactivity implies that enteric glia are widespread in the fish gastrointestinal tract.

3. Generation of transgenic zebrafish that express green fluorescent protein (GFP) in glial cells driven by the zebrafish glial fibrillary acidic protein (GFAP) regulatory elements.

4. Cells expressing the two reporters display radial glial morphology, colocalize with the NSC marker Sox2, undergo proliferation, and are capable of self-renewal within the matrix of distinct thickness in the telencephalon.