The recombinant human DLL3 protein is an active protein generated in mammalian cells. Its expression region corresponds to the 391-492aa of the human DLL3. The target gene is co-expressed with the C-terminal 10xHis-tag gene through a plasmid. The resulting DLL3 protein's purity is over 95% as measured by SDS-PAGE. In a functional ELISA, this human DLL3 protein can bind to the DLL3 recombinant antibody (CSB-RA882142MA2HU), with the EC50 of 1.107-1.282 ng/mL.
DLL3 is a Notch ligand that plays a crucial role in various cellular processes, particularly in the development and progression of certain types of cancer [1-6]. DLL3 is primarily localized in the Golgi apparatus and is rarely expressed on the cell surface [7][8]. Unlike other Notch ligands, DLL3 does not activate Notch receptors on neighboring cells. Instead, it can suppress the Notch signaling in a cell-autonomous manner by targeting newly synthesized Notch1 or DLL1 for endosomal/lysosomal degradation [8][9].
DLL3 is highly expressed in various types of cancer, particularly in small cell lung cancer (SCLC), neuroendocrine tumors, and some other neuroendocrine-like cancers [1-6]. High DLL3 expression is often associated with tumor growth, invasion, and metastasis, as well as poor patient prognosis [1][3][5][6]. DLL3 has been shown to regulate the conversion between mesenchymal and epithelial states, which is a crucial process in cancer metastasis [1].
DLL3 may interact with immune-related proteins, such as LG3BP and HSPA8, which regulate immune response [9]. However, the exact mechanisms by which DLL3 modulates the immune system are not yet fully understood. Due to its specific expression in certain types of cancer, DLL3 has emerged as a promising therapeutic target. Several DLL3-targeted therapies, including antibody-drug conjugates, bispecific T-cell engagers, and chimeric antigen receptor T cells, are currently under development and investigation for the treatment of DLL3-positive cancers [2][6][10][11].
References:
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[8] Y. Mizuno, K. Maemura, Y. Tanaka, A. Hirata, S. Futaki, H. Hamamoto, et al. Expression of delta-like 3 is downregulated by aberrant dna methylation and histone modification in hepatocellular carcinoma, Oncology Reports, 2018. https://doi.org/10.3892/or.2018.6293
[9] J. Ye, J. Wen, D. Wu, B. Hu, M. Luo, Y. Lin, et al. Elevated dll3 in stomach cancer by tumor-associated macrophages enhances cancer-cell proliferation and cytokine secretion of macrophages, Gastroenterology Report, vol. 10, 2021. https://doi.org/10.1093/gastro/goab052
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