DLL3 Specific Neutra™ Antibody Products
Product listDelta Like Canonical Notch Ligand 3 (DLL3) is important in the Notch signaling pathway, primarily regulating cell differentiation and developmental processes. DLL3 is particularly crucial during embryonic development, and its absence can lead to severe neurological and skeletal developmental defects. In small-cell lung cancer (SCLC), DLL3 is typically overexpressed and is associated with high aggressiveness and poor prognosis. Due to its specific overexpression, DLL3 has become a potential target for SCLC-targeted therapy research. Therefore, DLL3 holds significant biological and clinical importance in cancer treatment.
Its Gene ID: 10683, UniProtKB ID: Q9NYJ7, and OMIM ID: 602768.
DLL3 and Notch Signaling
Canonical Notch signaling is propelled by direct interactions between cell membrane-bound receptors Notch1-4 and ligands Jagged1, Jagged2, DLL1, DLL3, or DLL4. Additionally, the pathway can be non-canonically activated through other signaling pathways such as NF-κB, Wnt, TGF-β, and STAT3, as shown in Fig.1. Notch signaling plays a vital role in orchestrating hematopoiesis, guiding immune cell differentiation, and modulating inflammation. Furthermore, it is implicated in a spectrum of autoimmune conditions and contributes to the establishment of immunosuppression in tumor microenvironments. Mutations in Notch signaling are closely linked to a range of genetic disorders and cancers, playing diverse roles depending on the context.
Fig.1 The Notch pathway is regulated by short-range cell-cell signaling.1, 3
DLL3-Targeted Antibodies in Therapeutics
DLL3, an inhibitory Notch ligand, exhibits heightened expression levels in SCLC and other neuroendocrine tumors, contrasting with its minimal expression in normal tissues. This distinct expression pattern positions DLL3 as a promising therapeutic target in SCLC. The promising approach involves T cell-redirecting therapies that target DLL3-positive tumors. These therapies utilize a bispecific molecule that binds to both DLL3 on tumor cells and CD3 on endogenous T cells. This dual binding forms a cytolytic synapse, leading to antigen-dependent lysis of the target cells, activation of T cells, and production of cytokines. Remarkably, this mechanism operates independently of a specific T cell receptor or peptide-MHC complex, presenting a potential avenue to counteract the immunosuppressive milieu commonly found in tumors.
Fig.2 The mechanisms of action of DLL3 & CD3 bispecific antibody.2, 3
Services
Creative Biolabs stands at the forefront of biotechnology, excelling in the development and manufacture of premium recombinant antibodies. Our extensive array encompasses a diverse selection of anti-DLL3 antibodies meticulously crafted for an array of research and therapeutic endeavors. For further insights into our reliable anti-DLL3 antibody offerings, we invite you to contact us and explore our comprehensive product line. Let Creative Biolabs be your trusted partner in advancing your scientific discoveries.
REFERENCES
- Janghorban, Mahnaz, et al. "Notch signaling as a regulator of the tumor immune response: to target or not to target?" Frontiers in immunology 9 (2018): 373126.
- Owen, Dwight H., et al. "DLL3: an emerging target in small cell lung cancer." Journal of hematology & oncology 12 (2019): 1-8.
- Under open access license CC BY 4.0, without modification.
