Overview
- Peptide (C)RHLGTIPRLSLSR, corresponding to amino acid residues 27-39 of rat Glial fibrillary acidic protein (Accession P47819). Intracellular, cytoplasm.
GFAP Blocking Peptide (#BLP-FP001)
Expression of GFAP in rat hippocampus.Immunohistochemical staining of perfusion-fixed frozen rat brain sections with Anti-GFAP-ATTO Fluor-647N Antibody (#AFP-001-FRN), (1:100). A. Staining in the hippocampal CA3 region, shows GFAP immunoreactivity (purple) in astrocyte profiles in the stratum radiatum of CA3 (arrows). B. Pre-incubation of the antibody with GFAP Blocking Peptide (BLP-FP001), suppressed staining. Cell nuclei are stained with DAPI (blue).
Expression of GFAP in rat hippocampus.Immunohistochemical staining of perfusion-fixed frozen rat brain sections with Anti-GFAP-ATTO Fluor-647N Antibody (#AFP-001-FRN), (1:80). A. Staining in the hippocampal dentate gyrus region, shows GFAP immunoreactivity (purple) in astrocytes (arrows). B. Staining of sequential sections with Rabbit IgG Isotype Control-ATTO Fluor-647N (#RIC-001-FRN), (1:80), shows background signal. Cell nuclei are stained with DAPI (blue). H = hilus, G = granule layer, OML = outer molecular layer.
Expression of GFAP in rat cerebellum and hypothalamus.Immunohistochemical staining of perfusion-fixed frozen rat brain sections with Anti-GFAP-ATTO Fluor-647N Antibody (#AFP-001-FRN), (1:80). A. Staining in the cerebellum, shows GFAP immunoreactivity (purple) appearing along the Bergmann glial processes (arrows point at examples). B. Staining in the ventromedial hypothalamus region, shows GFAP immunoreactivity (purple), in astrocytes. Cell nuclei are stained with DAPI (blue). 3rd V = third cerebral ventricle. VMH = ventromedial hypothalamus.
Expression of GFAP and 5HT1B Receptor in rat hippocampus CA3 region.Immunohistochemical staining of perfusion-fixed frozen rat brain sections with Anti-GFAP-ATTO Fluor-647N Antibody (#AFP-001-FRN), (1:80) and Anti-5HT1B Receptor (HTR1B) (extracellular)-ATTO Fluor-488 Antibody (#ASR-022-AG), (1:80). A. GFAP immunoreactivity (purple) appears in astrocytes, but not in neurons (down pointing arrows). B. 5HT1B immunoreactivity (green) appears in neuronal apical dendrites, but not in astrocytes (horizontal arrows). C. Merge of the two images confirms differential staining of astrocytes and neurons. Cell nuclei are stained with DAPI (blue).
Expression of GFAP and TSH Receptor in rat hippocampus CA1 region.Immunohistochemical staining of perfusion-fixed frozen rat brain sections with Anti-GFAP-ATTO Fluor-647N Antibody (#AFP-001-FRN), (1:80) and Anti-TSH Receptor (TSHR) (extracellular)-ATTO Fluor-488 Antibody (#ATR-006-AG), (1:80). A. GFAP immunoreactivity (purple) appears in astrocytes (arrows). B. TSHR immunoreactivity (green) appears in astrocytic processes (arrows). C. Merge of the two images confirms specific astrocytic staining. Cell nuclei are stained with DAPI (blue).
Expression of GFAP in rat C6 glioma cellsFixed and permeabilized cells were stained with Anti-GFAP-ATTO Fluor-647N Antibody (#AFP-001-FRN), (1:200) and with CellMask Orange Actin tracking dye (yellow). Cell nuclei were stained with Hoechst 33342 (blue).
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Glial fibrillary acidic protein (GFAP) is a key intermediate filament (IF) III protein responsible for maintaining the mechanical strength of glia cells by supporting their cytoskeleton structure. GFAP is expressed in astrocytes in the CNS, non-myelinating Schwann cells in the PNS, and enteric glial cells1.
GFAP has a structural organization that is typical to class III IF proteins: it has a head, rod, and tail domains. The N-terminal head domain is important for filament formation and the C-terminal domain is important for oligomerization2.
GFAP is encoded by a single gene mapped to human chromosome 17q21. To date, 10 isoforms/splice variants have been identified. GFAP is tightly regulated: both at mRNA transcription level and by phosphorylation and other post-translational modifications. A number of growth factors such as CNTF, FGF and TGF-β can induce GFAP gene transcription activation leading to increased GFAP protein levels3.
Single nucleotide polymorphism (SNP) in GFAP results in the formation of Rosenthal fibers that cause Alexander Disease, hence, GFAP is a potential drug target for the treatment of this disease. A number of GFAP mutations were found in the coding and in the promoter regions of Alexander disease patients4.
GFAP gene activation and protein induction appear to play a critical role in astroglia cell activation (astrogliosis) following CNS injuries and neurodegeneration. GFAP protein and its breakdown products are rapidly released into biofluids following traumatic brain and spinal cord injuries and stroke, making them strong candidate biomarkers for such neurological disorders5.
Anti-GFAP Antibody (#AFP-001) is a highly specific antibody directed against an epitope of the rat GFAP protein. The antibody can be used in western blot and immunohistochemistry applications. It has been designed to recognize GFAP from rat and mouse samples. The antibody will not recognize human GFAP.
Anti-GFAP-ATTO Fluor-647N Antibody (#AFP-001-FRN) is directly conjugated to the ATTO Fluor-647N fluorophore. This conjugated antibody has been developed to be used in immunofluorescent applications such as multicolor immunohistochemistry and immunocytochemistry. It has been designed to recognize GFAP from mouse and rat samples. The antibody will not recognize human GFAP.
ATTO Fluor 647N belongs to a new generation of fluorescent labels for the red spectral region. Characteristic features of the label are strong absorption, high fluorescence quantum yield, high thermal and photo-stability, and exceptionally high stability towards atmospheric ozone. Thus ATTO Fluor 647N is highly suitable for single-molecule detection applications and super-resolution microscopy techniques such as Structured Illumination Microscopy (SIM), Stimulated Emission Depletion (STED), etc.
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