Product nameHuman EphA2 Antibody Pair - BSA and Azide free
See all Eph receptor A2 kits
Assay typeELISA set
Range7.81 pg/ml - 500 pg/ml
Species reactivityReacts with: Human
The Antibody Pair can be used to quantify Human EphA2. 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.
For additional information on the performance of the antibody pair, see the equivalent SimpleStep ELISA® Kit (ab219051), which uses the same antibodies. Please note that the range provided for the pairs is only an estimation based on the performance of the related product using the same antibody pair. Performance of the antibody pair will depend on the specific characteristics of your assay. We guarantee the product works in sandwich ELISA, but we do not guarantee the sensitivity or dynamic range of the antibody pair in your assay.
To receive an electronic copy of the Certificate of Analysis, please send an email to technical support with "CoA for matched antibody pair kit" in the subject line and the desired product number and lot number in the body of the email.
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Tested applicationsSuitable for: ELISAmore details
Storage instructionsStore at +4°C. Please refer to protocols.
Components 10 x 96 tests Human EphA2 Capture Antibody 1 x 100µg Human EphA2 Detector Antibody 1 x 100µg
FunctionReceptor for members of the ephrin-A family. Binds to ephrin-A1, -A3, -A4 and -A5. Plays an important role in angiogenesis and tumor neovascularization. The recruitement of VAV2, VAV3 and PI3-kinase p85 subunit by phosphorylated EPHA2 is critical for EFNA1-induced RAC1 GTPase activation and vascular endothelial cell migration and assembly (By similarity). Induces apoptosis in a p53/TP53-independent, caspase-8-dependent manner.
Tissue specificityExpressed in brain and glioma tissue and glioma cell lines (at protein level). Expressed most highly in tissues that contain a high proportion of epithelial cells, e.g., skin, intestine, lung, and ovary.
Involvement in diseaseGenetic variations in EPHA2 are the cause of susceptibility to cataract cortical age-related type 2 (ARCC2) [MIM:613020]. A developmental punctate opacity common in the cortex and present in most lenses. The cataract is white or cerulean, increases in number with age, but rarely affects vision.
Defects in EPHA2 are the cause of cataract posterior polar type 1 (CTPP1) [MIM:116600]. A subcapsular opacity, usually disk-shaped, located at the back of the lens. It can have a marked effect on visual acuity.
Sequence similaritiesBelongs to the protein kinase superfamily. Tyr protein kinase family. Ephrin receptor subfamily.
Contains 2 fibronectin type-III domains.
Contains 1 protein kinase domain.
Contains 1 SAM (sterile alpha motif) domain.
modificationsActivated by EFNA1 via tyrosine phosphorylation. Phosphorylated residues Tyr-588 and Tyr-594 are required for binding VAV2 and VAV3 while phosphorylated residues Tyr-735 and Tyr-930 are required for binding PI3-kinase p85 subunit. These phosphorylated residues are critical for recruitment of VAV2 and VAV3 and PI3-kinase p85 subunit which transduce downstream signaling to activate RAC1 GTPase and endothelial cell migration. They also play a critical role in transducing EPHA2 signaling in vascular endothelial cells during tumor angiogenesis.
- Information by UniProt
Our Abpromise guarantee covers the use of ab241804 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ELISA||Use at an assay dependent concentration.|
ab241804 has not yet been referenced specifically in any publications.