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B6-huDLL3 Mouse
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B6-huDLL3 Mouse
Product Name
B6-huDLL3 Mouse
Product ID
C001854
Strain Name
C57BL/6NCya-Dll3tm1(hDLL3)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “B6-huDLL3 Mouse (Catalog C001854) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
The standard delivery applies for a guaranteed minimum of three heterozygous carriers. Breeding services for homozygous carriers and/or specified sex are available.
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Basic Information
Related Resource
Basic Information
Gene Name
DLL3
Gene Alias
SCDO1
NCBI ID
Chromosome
Chr 19 (Human)
MGI ID
Datasheet
Strain Description
The DLL3 (Delta-like canonical Notch ligand 3) gene encodes a transmembrane protein belonging to the Delta/Serrate/Lag-2 (DSL) family of ligands. Functioning within the highly conserved Notch signaling pathway, DLL3 exhibits a unique, inhibitory role, contrasting with the canonical activating function of other Notch ligands. It is believed to antagonize Notch signaling by preventing ligand-receptor interactions or by promoting receptor degradation, a mechanism critical for establishing proper cell fate decisions during development [1]. This is particularly evident in the formation of somites, where DLL3's function is essential for the rhythmic segmentation of the presomitic mesoderm [2]. While its expression is largely restricted to fetal tissues and progenitor cells in healthy adults, DLL3 is ectopically and highly expressed in a number of neuroendocrine tumors, including small cell lung cancer (SCLC), making it a promising therapeutic target. Pathogenic variants in the DLL3 gene are directly linked to Spondylocostal dysostosis type 1, a congenital disorder of vertebral segmentation [3].
The B6-huDLL3 mice are a humanized model constructed through gene editing technology, in which the mouse Dll3 endogenous extracellular domain is replaced with the human DLL3 extracellular domain. The murine signal peptide and transmembrane-cytoplasmic region are preserved. This model can be used for the study of the pathological mechanisms and treatment methods of DLL3-highly-expressed malignant tumors and Spondylocostal dysostosis type 1. It can also be applied to the development of DLL3-targeted drugs.
Reference
Furuta M, Kikuchi H, Shoji T, Takashima Y, Kikuchi E, Kikuchi J, Kinoshita I, Dosaka-Akita H, Sakakibara-Konishi J. DLL3 regulates the migration and invasion of small cell lung cancer by modulating Snail. Cancer Sci. 2019 May;110(5):1599-1608.
Ramesh PS, Chu LF. Species-specific roles of the Notch ligands, receptors, and targets orchestrating the signaling landscape of the segmentation clock. Front Cell Dev Biol. 2024 Jan 29;11:1327227.
Umair M, Younus M, Shafiq S, Nayab A, Alfadhel M. Clinical genetics of spondylocostal dysostosis: A mini review. Front Genet. 2022 Nov 25;13:996364.
Strain Strategy

Figure 1. Gene editing strategy of B6-huDLL3 mice. The mouse Dll3 endogenous extracellular domain is replaced with the human DLL3 extracellular domain. The murine signal peptide and transmembrane-cytoplasmic region are preserved.
Application Area
Screening, development, and evaluation of DLL3-targeted drugs;
Research on the pathological mechanisms and treatment methods of Spondylocostal dysostosis type 1;
Research on the pathological mechanisms and treatment methods of DLL3-highly-expressed malignant tumors.
Related Resource
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