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BRAND / VENDOR: Abcam

Abcam, ab256906, Human ENG (CD105) knockout HeLa cell lysate

CATALOG NUMBER: ab256906
السعر العادي$0.99
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Product Description

Size: 1Kit
ENG KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 11 bp deletion in exon2 and 19 bp deletion in exon2 and 1 bp insertion in exon2.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 11 bp deletion in exon2 and 19 bp deletion in exon2 and 1 bp insertion in exon2.,
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-ENG, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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.
CD105 also known as endoglin or the CD105 marker is a transmembrane glycoprotein with a molecular weight of approximately 180 kDa. It is a component of the TGF-beta receptor complex and exists in endothelial cells where it is abundantly expressed. Expression of CD105 is higher in proliferating cells particularly in the vasculature. You can also find it in tissues involved in the formation and remodeling of blood vessels such as during angiogenesis.
Biological function summary
Endoglin functions in the regulation of angiogenesis and vascular remodeling. It plays a significant role in mediating cellular responses to TGF-beta signaling influencing endothelial cell proliferation and migration. While not part of a larger structural complex endoglin interacts with receptors and signaling molecules important for vascular development and repair processes. This involvement aids in maintaining endothelial integrity and function under various physiological conditions.
Pathways
CD105 participates in the TGF-beta signaling and angiogenesis pathways. In these pathways it acts in conjunction with other proteins like TGF-beta receptors which play roles in cell differentiation proliferation and apoptosis. The interaction between CD105 and TGF-beta signaling regulates numerous cellular mechanisms impacting angiogenesis and cellular responses to environmental changes.
CD105 has links to hereditary hemorrhagic telangiectasia (HHT) and certain cancers. In HHT mutations in the endoglin gene alter vascular structure leading to the formation of abnormal blood vessels. Oncologically overexpression of CD105 is present in tumor angiogenesis aiding in the progression of certain cancers. Other proteins like VEGF and TGF-beta closely interact with endoglin influencing disease progression and presenting potential targets for therapeutic intervention.


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Collaboration

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