The DLK2 Knockout HEK293T Polyclonal Cells are a polyclonal CRISPR/Cas9-edited population with targeted disruption of the DLK2 gene in the HEK293T host background. This product provides a heterogeneous knockout model for studying the non-canonical Notch ligand DLK2, which negatively regulates canonical Notch signaling by competing with DLL/JAG ligands for receptors such as NOTCH1 and NOTCH2. The polyclonal format offers a robust platform for functional analyses without clonal isolation.
HEK293T is a widely utilized human embryonic kidney epithelial line transformed with SV40 large T-antigen, facilitating episomal plasmid replication and efficient transfection. These adherent cells are an established host for protein expression, lentivirus production, and transient gene delivery. Their endogenous expression of core signaling elements allows probing of pathways perturbed by strategic gene knockouts, as with this DLK2-disrupted population.
DLK2 is a non-canonical Notch ligand that antagonizes signaling by competing with canonical ligands DLL1 and JAG1 for receptor binding, repressing targets HES1 and HEY1. Its expression is controlled by adipogenic factors PPARG, CEBPA, and SREBF1, and it impacts metabolic genes such as ADIPOQ and FABP4. This places DLK2 at the intersection of Notch and adipogenic/insulin pathways, where it modulates glucose homeostasis and adipogenesis.
Within HEK293T cells, knockout of DLK2 relieves tonic inhibition of Notch signaling, enhancing HES/HEY transcription and potentially altering metabolic regulatory networks. Because these cells express key adipogenic regulators, they enable investigation of DLK2??s role in repressing adipogenesis-associated programs. This disruption therefore allows study of how de-repressed Notch activity influences lipid and glucose metabolism in a human epithelial context.
This loss-of-function model is compatible with Notch luciferase reporter assays, RT-qPCR for HES1 and HEY1, western blotting for DLK2, NOTCH1, and HES1, and adipogenic differentiation with Oil Red O staining followed by RNA-seq profiling. These applications support mechanistic studies in obesity, type 2 diabetes, and drug screening for metabolic syndrome. For additional details, please contact Ascent Research.
