>CD24 & Siglec-10 Proteins - Hot Targets for Tumor Immunother
Cancer cells are capable of evading clearance by macrophages through the overexpression of anti-phagocytic surface proteins called "don't eat me" signals - including CD47, PD-L1 and B2M. The study published in Nature in July 2019  showed that CD24 is another "don't eat me" signal expressed by ovarian cancer and triple-negative breast cancer cells.
CD24 is a sialoglycoprotein expressed at the surface of most B lymphocytes and differentiating neuroblasts. The encoded protein is anchored via a glycosyl phosphatidylinositol (GPI) link to the cell surface. The protein also contributes to a wide range of downstream signaling networks and is crucial for neural development. Cross-linking of CD24 on the surface of neutrophils induces apoptosis, and this appears to be defective in sepsis. CD24 can promoting immune evasion through its interaction with the inhibitory receptor Siglec-10, which is expressed by tumor-associated macrophages.
Most of CD24 proteins on the market only have data of binding to anti-CD24 antibodies, but didn’t verify the interaction of CD24 and Siglec-10. CD24 is the biomarker of ovarian cancer and triple-negative breast cancer cells. It is important to verify the binding signal of Siglec-10 to CD24 on the surface of tumor cells. And the key point of CD24 antibody drug development is that it can effectively block the binding of CD24 and Siglec-10.
ACROBiosystems has developed CD24 protein with different tags and CD24 overexpressed cells. The binding activity of CD24 overexpressed cells and Siglec-10 was verified by FACS. The binding signal of Siglec-10 and CD24 overexpressed cells was inhibited by anti-CD24 neutralizing antibody (SN3), and the FACS protocols are offered.
|Molecule||Cat. No.||Host||Product Description||Structure|
Fig.1 FACS assay showed that Human Siglec-10 can bind to CD24 overexpressed cells.
Fig.2 FACS assay showed that the binding signal of Siglec-10 and CD24 overexpressed cells was inhibited by anti-CD24 neutralizing antibody.
Authors: Barkal AA, et al.
Journal: Nature. 2019.
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