The CCDC14 Knockout Raji Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population for studying the centrosomal protein CCDC14. Generated by target-gene disruption in the Raji B-lymphocyte line, this model offers a versatile loss-of-function system to investigate CCDC14??s roles in ciliogenesis, cell cycle regulation, and microtubule organization without the constraints of clonal variability.
Raji cells, derived from a Burkitt lymphoma patient, constitute an EBV-positive lymphoblastoid line that retains B-cell functions such as antibody production and antigen presentation. Widely employed in immunology and oncology research, this cell line serves as a robust platform for examining B-cell malignancies and immune response mechanisms, particularly in the context of centrosomal protein functions and signaling pathway alterations.
CCDC14 localizes to the centrosome and is essential for normal ciliogenesis and cell cycle progression. It is regulated by cell cycle-dependent kinases, notably Aurora A and PLK1, and interacts with centrosomal scaffold proteins including CEP290 and PCM1. CCDC14 functions upstream of microtubule-associated proteins and intraflagellar transport components such as IFT88, influencing both Hedgehog signaling via the transcription factor GLI1 and Wnt/??-catenin signaling through CTNNB1. Disruption of CCDC14 impairs proper centrosome-mediated microtubule organization and alters downstream ciliary and mitotic pathways.
In Raji B-lymphoma cells, knockout of CCDC14 is anticipated to compromise centrosome-dependent regulation of the cell cycle and microtubule dynamics, potentially leading to aberrant proliferation, altered immune signaling, and disrupted antigen presentation. Although mature B lymphocytes typically lack primary cilia, centrosomal proteins critically influence cell division and signaling cascades; thus, this model may uncover CCDC14-dependent crosstalk between Hedgehog and Wnt pathways in lymphomagenesis, providing insights into centrosome-related vulnerabilities in B-cell malignancies.
Researchers can utilize this polyclonal knockout population for immunofluorescence-based analysis of centrosomal markers to assess structural integrity, Western blotting to confirm CCDC14 loss, and flow cytometry for cell cycle profiling. Proliferation assays and drug sensitivity screens facilitate the identification of compounds targeting centrosomal pathways or mitotic kinases. Additionally, these cells enable functional interrogation of CCDC14 in Hedgehog and Wnt signaling contexts relevant to lymphoma biology. For more information, please contact Ascent Research.
