Human/Mouse GFAP Antibody Pair - BSA and Azide free (RMAB-0252038)
Cat. No.: RMAB-0252038
Category: Antibody Pair
INQUIRY
10 x 96 tests
The Antibody Pair can be used to quantify Human/Mouse GFAP. BSA and Azide free antibody pairs include unconjugated capture and detector antibodies suitable for sandwich ELISAs. The antibodies are provided at an approximate concentration of 1 mg/mL as measured by the protein A280 method. The recommended antibody orientation is based on internal optimization for ELISA-based assays. Antibody orientation is assay dependent and needs to be optimized for each assay type. Both capture and detector antibodies are rabbit monoclonal antibodies delivering consistent, specific, and sensitive results._x000D_
Product Features
| Conjugate | Unconjugated capture and detector antibodies |
|---|---|
| Species Reactivity | Mouse, Human |
| Range | 125 pg/mL - 8000 pg/mL |
| Applications | Sandwich ELISA |
| Key Features | Unconjugated capture and detector antibodies; Adaptable to any antibody pair-based assay format; Antibody concentration ~ 1 mg/mL; BSA and azide free buffer - ready for conjugation; Reacts with: Mouse, Human |
Target Information
| Target Symbol | GFAP |
|---|---|
| Target Name | Glial fibrillary acidic protein |
| UniProt ID | P14136 |
| Cellular Localization | Cytoplasm. Associated with intermediate filaments. |
| Function | GFAP, a class-III intermediate filament, is a cell-specific marker that, during the development of the central nervous system, distinguishes astrocytes from other glial cells. |
| Involvement in Disease | Defects in GFAP are a cause of Alexander disease (ALEXD). Alexander disease is a rare disorder of the central nervous system. It is a progressive leukoencephalopathy whose hallmark is the widespread accumulation of Rosenthal fibers which are cytoplasmic inclusions in astrocytes. The most common form affects infants and young children, and is characterized by progressive failure of central myelination, usually leading to death usually within the first decade. Infants with Alexander disease develop a leukoencephalopathy with macrocephaly, seizures, and psychomotor retardation. Patients with juvenile or adult forms typically experience ataxia, bulbar signs and spasticity, and a more slowly progressive course. |
| Post-translational Modifications | Phosphorylated by PKN1. |
| Sequence Similarities | Belongs to the intermediate filament family. |
Storage & Shipping
| Storage & Shipping | Store at 4°C. Please refer to protocols. |
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For research use only. Not for clinical use.
