CSPP1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphoblastoid cell line, featuring targeted disruption of the CSPP1 gene. This product provides a genetically heterogeneous pool of cells with inactivated CSPP1, enabling functional studies without prior clonal isolation. The polyclonal format retains diverse editing events, making it ideal for pooled loss-of-function assays and phenotypic screening.
The Raji host cell line originates from a human Burkitt lymphoma and exhibits typical B lymphocyte characteristics, including robust antibody production, immune surveillance functions, and antigen presentation capabilities. As a well-characterized model for B-cell biology and lymphomagenesis, Raji cells provide a physiologically relevant context for investigating centrosome-related processes in a malignant, actively dividing lymphocyte background. Their rapid proliferation and well-defined signaling networks facilitate the study of cell cycle regulation and cytoskeletal dynamics.
CSPP1 encodes a centrosome- and spindle pole-associated protein critical for microtubule organization during mitosis and primary cilium formation. It functions downstream of mitotic kinases CDK1, PLK1, and Aurora A, which regulate its localization and activity. CSPP1 directly interacts with PCM1, tubulin, and multiple CEP proteins to promote microtubule nucleation and stabilization. Disruption of CSPP1 leads to defective centrosome duplication, spindle pole organization, and ciliogenesis, resulting in aberrant mitotic spindle assembly, chromosome missegregation, and impaired ciliary signaling, ultimately compromising cell cycle progression and proliferation.
In the Raji B-cell context, CSPP1 knockout is particularly relevant for dissecting the relationship between centrosome integrity and malignant transformation. Aberrant centrosome numbers and defective spindles are common in cancer, and CSPP1 disruption in these rapidly dividing lymphocytes can reveal mechanisms of chromosomal instability in lymphoma. Moreover, primary cilia dysfunction in this model aids in understanding how ciliopathy-related pathways contribute to B-cell pathology, including insights into Joubert syndrome, a disorder linked to CSPP1 mutations.
These polyclonal knockout cells are well-suited for a variety of experimental approaches, including immunofluorescence microscopy to assess centrosome and cilia markers, flow cytometry for cell cycle analysis, western blotting to confirm CSPP1 protein depletion, and RT-qPCR to measure CSPP1 mRNA levels. EdU proliferation assays can evaluate changes in cell growth kinetics. The model supports research in centrosome biology, ciliopathy modeling, cell cycle studies, and cancer cell biology, providing a robust platform for mechanistic investigations and drug discovery screens. For further information and technical support, please contact Ascent Research.
