Recombinant Human Delta-like protein 3 (DLL3), partial (Active) CSB-MP882142HU2 CUSABIO
$9.90
In stock
SKU
CSB-MP882142HU2
Product Details
| Uniprot No. | Q9NYJ7 |
| Alternative Names | Delta-like protein 3; Drosophila Delta homolog 3 (Delta3) |
| Species | Homo sapiens (Human) |
| Source | Mammalian cell |
| Expression Region | 429-492aa |
| Purity | Greater than 95% as determined by SDS-PAGE. |
| Activity | Measured by its binding ability in a functional ELISA. Immobilized Human DLL3 at 1 μg/mL can bind Anti-DLL3 recombinant antibody (CSB-RA882142MA2HU). The EC50 is 6.211-7.209 ng/mL. |
| Tag Info | C-terminal mFc-tagged |
| Form | Lyophilized powder Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand. |
| Buffer | Lyophilized from a 0.2 μm filtered PBS, 6% Trehalose, pH 7.4 |
| Reconstitution | We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference. |
| Troubleshooting and FAQs | Protein FAQs |
| Notes | Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week. |
| Lead Time | 3-7 business days |
| Target Names | DLL3 |
| Target Protein Sequence | RADPCAARPCAHGGRCYAHFSGLVCACAPGYMGARCEFPVHPDGASALPAAPPGLRPGDPQRYL |
| Mol. Weight | 36.0kDa |
| Protein Length | Partial |
| Storage Condition | Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles. |
| Shelf Life | The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C. |
| Datasheet & COA | Please contact us to get it. |
| Description | The recombinant human DLL3 protein is produced by transfecting mammalian cells with a plasmid containing the gene segment encoding the 429-492aa region of the human DLL3. The target gene segment is co-expressed with the C-terminal mFc-tag gene. SDS-PAGE analysis verifies a purity level of this DLL3 protein above 95%. The functional activity of this recombinant DLL3 protein is validated through ELISA, with specific DLL3 recombinant antibody (CSB-RA882142MA2HU) binding showing an EC 50 range of 6.211 to 7.209 ng/mL. Human DLL3 is a member of the Delta/Serrate/LAG-2 (DSL) family of proteins, which play critical roles in the Notch signaling pathway. Unlike other DSL ligands, DLL3 does not activate Notch signaling but instead acts as a negative regulator, inhibiting the signaling induced by other DSL ligands such as DLL1 [1][2]. This unique function positions DLL3 as a significant player in various biological processes, particularly in neurogenesis and the development of certain cancers. DLL3 is predominantly expressed in neuroendocrine tumors, especially small cell lung cancer (SCLC), where it serves as a potential biomarker and therapeutic target. Studies have shown that DLL3 is highly expressed in SCLC, with approximately 72% of treatment-naïve cases exhibiting positive DLL3 expression [3][4]. Furthermore, DLL3 expression is associated with poor prognosis in various cancers, including endometrial cancer and small cell bladder cancer, where high levels of DLL3 correlate with shorter progression-free survival (PFS) and overall survival (OS) [5][6]. In addition to its role in cancer, DLL3 mutations are implicated in spondylocostal dysostosis (SCD), a genetic disorder characterized by vertebral segmentation defects. Mutations in the DLL3 gene disrupt normal somitogenesis, leading to various skeletal deformities [7-9]. These mutations can result in truncated proteins that fail to function properly, thereby affecting the Notch signaling pathway, which is essential for proper vertebral development [10][11]. References: [1] E. Ladi, J. Nichols, W. Ge, A. Miyamoto, C. Yao, L. Yang, et al. The divergent dsl ligand dll3 does not activate notch signaling but cell autonomously attenuates signaling induced by other dsl ligands, The Journal of Cell Biology, vol. 170, no. 6, p. 983-992, 2005. https://doi.org/10.1083/jcb.200503113 [2] I. Geffers, K. Serth, G. Chapman, R. Jaekel, K. Schuster-Gossler, R. Cordes, et al. Divergent functions and distinct localization of the notch ligands dll1 and dll3 in vivo, The Journal of Cell Biology, vol. 178, no. 3, p. 465-476, 2007. https://doi.org/10.1083/jcb.200702009 [3] M. Furuta, J. Sakakibara‐Konishi, H. Kikuchi, H. Yokouchi, H. Nishihara, H. Minemura, et al. Analysis of dll3 and ascl1 in surgically resected small cell lung cancer (hot1702), The Oncologist, vol. 24, no. 11, p. e1172-e1179, 2019. https://doi.org/10.1634/theoncologist.2018-0676 [4] D. Morgensztern, B. Besse, L. Greillier, R. Santana-Dávila, N. Ready, C. Hann, et al. Efficacy and safety of rovalpituzumab tesirine in third-line and beyond patients with dll3-expressing, relapsed/refractory small-cell lung cancer: results from the phase ii trinity study, Clinical Cancer Research, vol. 25, no. 23, p. 6958-6966, 2019. https://doi.org/10.1158/1078-0432.ccr-19-1133 [5] J. Wang, K. Zhang, Z. Li, T. Wang, F. Shi, Y. Zhang, et al. Upregulated delta-like protein 3 expression is a diagnostic and prognostic marker in endometrial cancer, Medicine, vol. 97, no. 51, p. e13442, 2018. https://doi.org/10.1097/md.0000000000013442 [6] V. Koshkin, J. García, J. Reynolds, P. Elson, C. Magi‐Galluzzi, J. McKenney, et al. Transcriptomic and protein analysis of small-cell bladder cancer (scbc) identifies prognostic biomarkers and dll3 as a relevant therapeutic target, Clinical Cancer Research, vol. 25, no. 1, p. 210-221, 2019. https://doi.org/10.1158/1078-0432.ccr-18-1278 [7] S. Dunwoodie, M. Clements, D. Sparrow, X. Sa, R. Conlon, & R. Beddington. Axial skeletal defects caused by mutation in the spondylocostal dysplasia/pudgy genedll3are associated with disruption of the segmentation clock within the presomitic mesoderm, Development, vol. 129, no. 7, p. 1795-1806, 2002. https://doi.org/10.1242/dev.129.7.1795 [8] P. Turnpenny, N. Whittock, J. Duncan, S. Dunwoodie, K. Kusumi, & S. Ellard. Novel mutations in dll3, a somitogenesis gene encoding a ligand for the notch signalling pathway, cause a consistent pattern of abnormal vertebral segmentation in spondylocostal dysostosis, Journal of Medical Genetics, vol. 40, no. 5, p. 333-339, 2003. https://doi.org/10.1136/jmg.40.5.333 [9] F. Khan, A. Arshad, A. Ullah, E. Steenackers, G. Mortier, F. Ahmad, et al. Identification of a novel nonsense variant in the dll3 gene underlying spondylocostal dysostosis in a consanguineous pakistani family, Molecular Syndromology, vol. 14, no. 3, p. 191-200, 2023. https://doi.org/10.1159/000527043 [10] L. Bonafé, C. Giunta, M. Gassner, B. Steinmann, & A. Superti‐Furga. A cluster of autosomal recessive spondylocostal dysostosis caused by three newly identified dll3 mutations segregating in a small village, Clinical Genetics, vol. 64, no. 1, p. 28-35, 2003. https://doi.org/10.1034/j.1399-0004.2003.00085.x [11] N. Whittock, S. Ellard, J. Duncan, C. Die-Smulders, J. Vles, & P. Turnpenny. Pseudodominant inheritance of spondylocostal dysostosis type 1 caused by two familial delta‐like 3 mutations, Clinical Genetics, vol. 66, no. 1, p. 67-72, 2004. https://doi.org/10.1111/j.0009-9163.2004.00272.x |
Reviews
Write Your Own Review
Related Products
Check items to add to the cart or
