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  • mProX™ Human DLL3 Stable Cell Line

    [CAT#: S01YF-1023-PY266]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:

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    Host Cell Type:
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    Product Information

    Target Family
    Other Targets
    Target Protein Species
    Human
    Host Cell Type
    HEK293;CHO-K1;SBC-5
    Target Classification
    Other Targets Drug Discovery Assays and Products
    Target Research Area
    Metabolic Research
    Related Diseases
    Spondylocostal Dysostosis 1, Autosomal Recessive; Spondylocostal Dysostosis, Autosomal Recessive
    Gene ID
    Human:10683
    UniProt ID
    Human:Q9NYJ7

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    DLL3, or delta-like ligand 3, is a protein that has been studied in various contexts. In a study on mice, it was found that Saikosaponin A (SSa), a component of Radix Bupleuri, activates the DLL3 signaling pathway and promotes neurogenesis in the hippocampus, potentially improving depression-like behavior. In ovarian cancer, the expression of DLL3 was found to be associated with clinical factors such as stage and race, and it was also linked to immune cell infiltration. In small-cell lung carcinoma, DLL3 expression was associated with different molecular subtypes of the disease, and it was found to impact the tumor microenvironment and the efficacy of anti-PD-L1 antibody plus chemotherapy. Additionally, in a case report, a variant in the TPM2 gene was identified in a patient with spondylospinal thoracic dysostosis, a rare genetic disorder that affects the spine and ribs. These studies highlight the diverse applications of DLL3 in various diseases and biological processes.

    Protocols

    Please visit our protocols page.

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    FAQ

    chat Casey Smith (Verified Customer)

    What is the role of DLL3 in small cell lung cancer (SCLC) therapy? Aug 02 2023

    chat Patrick Liam (Creative Biolabs Scientific Support)

    DLL3 is a promising target in SCLC therapy. Rovalpituzumab tesirine, a directed agent against DLL3, has shown potential in treating SCLC by controlling cell differentiation, proliferation, and survival. Aug 02 2023

    chat Peyton Johnson (Verified Customer)

    Can DLL3 be targeted in neuroendocrine carcinomas? Aug 20 2022

    chat Patrick Liam (Creative Biolabs Scientific Support)

    DLL3 is overexpressed in many neuroendocrine neoplasms (NENs) and is associated with poor clinical outcomes, especially in patients with neuroendocrine carcinoma (NEC), making it a clinically actionable target across NEN. Aug 20 2022

    Published Data

    Fig.1 Impact of overexpressing DLL3 on SBC-5 cell proliferation.

    The measurement of cell growth, both anchorage-dependent and anchorage-independent, was conducted using 96-well plates with or without poly-HEMA coating 72 hours after the seeding of SBC-5 cells. These cells had been transfected with either an empty vector or the DLL3-expression vector. The data was obtained from three independent experiments, and the results were expressed as mean ± SD.

    Ref: Furuta, Megumi, et al. "DLL 3 regulates the migration and invasion of small cell lung cancer by modulating Snail." Cancer Science 110.5 (2019): 1599-1608.

    Pubmed: 30874360

    DOI: 10.1111/cas.13997

    Research Highlights

    Tong, Yue. et al. "Saikosaponin a activates tet1/dll3/notch1 signalling and promotes hippocampal neurogenesis to improve depression-like behavior in mice." Journal of ethnopharmacology, 2023.
    In their study, researchers utilized a chronic social defeat stress (CSDS) mouse model to investigate the potential of SSa in alleviating depressive disorder in vivo. They established the CSDS mouse model and conducted various behavioral tests, including the social interaction test (SIT), sucrose preference test (SPT), forced-swim test (FST), tail suspension test (TST), and open field test (OFT). Furthermore, they employed Western blotting, immunofluorescence, and Golgi staining to examine signaling pathways and synaptic spine changes in the hippocampus. Molecular docking and microscale thermophoresis (MST) techniques were applied to explore the interaction between SSa and Tet1. Lentiviral transfection with sh-RNA Tet1 was used to validate Tet1's role in SSa efficacy in CSDS mice. The results demonstrated that SSa effectively reduced depressive symptoms, upregulated Tet1, Notch, DLL3, and BDNF expression, promoted hippocampal development, and increased dendritic spine density in hippocampal neurons. Notably, Tet1 knockdown in CSDS mice attenuated SSa's antidepressant effects, suggesting the importance of the Tet1/Notch/DLL3 signaling pathways and their potential as targets for novel antidepressant development.
    Tong, Yue. et al. "Saikosaponin a activates tet1/dll3/notch1 signalling and promotes hippocampal neurogenesis to improve depression-like behavior in mice." Journal of ethnopharmacology, 2023.
    Pubmed: 37844745   DOI: 10.1016/j.jep.2023.117289

    Chen, Buze. et al. "NOTCH Pathway Genes in Ovarian Cancer: Clinical Significance and Associations with Immune Cell Infiltration." Frontiers in bioscience (Landmark edition), 2023.
    The activation of the immune response is essential for host defense against pathogens. This process is mediated through a complex interplay of various immune cells, cytokines, and chemokines. Dysregulation of this system can result in a variety of diseases, including autoimmunity and immune deficiencies. In recent years, significant advancements have been made in our understanding of immune activation and its potential therapeutic applications. However, further research is required to fully elucidate the mechanisms involved and develop more effective treatments.
    Chen, Buze. et al. "NOTCH Pathway Genes in Ovarian Cancer: Clinical Significance and Associations with Immune Cell Infiltration." Frontiers in bioscience (Landmark edition), 2023.
    Pubmed: 37796700   DOI: 10.31083/j.fbl2809220

    Please note: All products are "FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR CLINICAL PROCEDURES" For licensing inquiries, please contact
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