Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 1 bp insertion in exon 5.,
Disease:Adenocarcinoma
Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-EPHA2, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Eph receptor A2 also known as EphA2 or A2 receptor is a type of protein that functions as a receptor tyrosine kinase. It has an approximate mass of 130 kDa. Researchers find this receptor widely expressed in various tissues including epithelial cells and some neuronal populations. EphA2 is involved in cell positioning movement and organization by interacting with ephrin ligands notably ephrin A1. The receptor-ligand interaction triggers bidirectional signaling that affects cell structure and function.
Biological function summary
Eph receptor A2 participates in important cellular processes such as angiogenesis cell proliferation and migration. It often functions as part of larger signaling networks or complexes that include other Eph receptors and ephrin ligands. These interactions help regulate cell adhesion and detachment which are important for embryonic development and tissue organization. EphA2 studies often use fluorescent labeling strategies such as Alexa 588 to track its expression and activity in cells.
Pathways
Eph receptor A2 integrates into the PI3K/AKT and MAPK signaling pathways which are important for cell survival growth and differentiation. It interacts with proteins like Ras and ERK within these pathways to modulate their functions. EphA2 signaling influences cytoskeletal dynamics and morphogenesis making it an important component in maintaining tissue architecture. Research also indicates a connection between EphA2 and the APC protein highlighting its role in the Wnt signaling pathway.
The Eph receptor A2 shows significant involvement in cancer and inflammatory conditions. Overexpression or dysregulation of EphA2 occurs frequently in various cancers including breast and prostate cancer correlating with increased tumor aggressiveness and metastasis. The receptor also interacts with other proteins such as APC which links to tumorigenesis and cancer progression. In immunology EphA2 plays a part in chronic inflammatory diseases by modulating immune cell migration and vascular inflammation. Understanding these connections provides insights for potential therapeutic targets using molecular interventions like A2 antibodies and APC-based strategies.
