The DCLK2 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited human polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line, engineered to disrupt the DCLK2 gene and create a loss-of-function model. This product enables the investigation of DCLK2-dependent cellular processes without introducing a single-cell clonal bias, preserving the inherent heterogeneity of the knockout pool. The polyclonal format is particularly suited for functional genomics screens and assays where population-level effects of DCLK2 disruption are analyzed, offering a versatile tool for researchers focused on microtubule-associated kinase signaling in lymphoma biology.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive, B lymphoblastoid model established from a Burkitt lymphoma patient. It carries the characteristic t(8;14) chromosomal translocation that juxtaposes the c-MYC oncogene with the immunoglobulin heavy chain locus, driving constitutive c-MYC expression and malignant proliferation. As a widely used B-cell lymphoma model, Raji cells exhibit rapid growth and retain key B-cell lineage features, making them an appropriate platform to dissect the contribution of DCLK2 to lymphomagenesis and cancer cell signaling within a defined oncogenic background.
DCLK2 encodes a serine/threonine protein kinase that associates with microtubules and functions as a critical regulator of ciliogenesis, cell migration, and proliferation. Mechanistically, DCLK2 transduces signals downstream of Wnt/??-catenin pathway activation, where TCF/LEF transcription factors promote its expression, and it subsequently influences ciliary maintenance by interacting with intraflagellar transport proteins such as IFT88 and IFT140. It also participates in Hedgehog signaling, acting upstream of Smoothened (Smo) and Gli transcription factors. In addition, DCLK2 forms complexes with the dynein motor complex and SMAD3, linking microtubule dynamics to transforming growth factor-?? (TGF-??) pathway components. Through these interactions, DCLK2 phosphorylates and regulates cytoskeletal regulators and SMAD2/3, thereby coordinating motile and proliferative responses.
In the context of Raji B lymphoblastoid cells, DCLK2 knockout disrupts microtubule-associated ciliary functions and impairs the integrated Wnt/??-catenin and Hedgehog signaling networks that are often aberrantly active in B-cell lymphoma. Loss of DCLK2 is expected to attenuate TCF/LEF-driven transcription, reduce Gli-mediated hedgehog target gene expression, and diminish ciliary-dependent proliferative cues. Consequently, this model may exhibit reduced cell migration and proliferation, reflecting the kinase??s role in sustaining oncogenic signaling. The EBV-positive, c-MYC-driven background provides a clinically relevant setting to assess how DCLK2 loss modulates lymphoma cell behavior in the presence of established oncogenic drivers.
Researchers can utilize the DCLK2 Knockout Raji Polyclonal Cells in diverse experimental workflows, including Western blotting to confirm DCLK2 protein ablation, RT-qPCR to quantify target gene expression, and immunofluorescence staining for acetylated ??-tubulin to visualize ciliary structures. Functional assays such as transwell migration, Annexin V apoptosis flow cytometry, and Wnt/??-catenin or Hedgehog Gli-responsive luciferase reporter assays are directly applicable to characterize signaling outputs. These cells are ideal for identifying DCLK2-dependent drug sensitivities via compound screening and for conducting comparative proliferation studies. For further information, please contact Ascent Research.
