CENPB Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population from the Raji B-lymphocyte line. The product is generated by CRISPR/Cas9-mediated gene disruption of CENPB, creating a heterogeneous knockout pool. This polyclonal format avoids clonal artifacts and preserves population diversity, suitable for bulk knockout studies. As a loss-of-function model, these cells enable dissection of CENPB roles in centromere function and mitotic fidelity.
The Raji host cell line is an EBV-positive lymphoblastoid line derived from Burkitt lymphoma. Raji cells proliferate rapidly and serve as a model for B-cell biology, lymphoma pathogenesis, and immune cell studies. Their well-characterized karyotype and B-cell marker expression facilitate chromosomal dynamics and oncogenic research. The EBV background provides a relevant system to study centromere dysfunction in lymphomagenesis and genomic instability in B cells.
CENPB encodes centromere protein B, which binds the 17-bp CENP-B box in centromeric alpha-satellite DNA. Regulated by CDK1 phosphorylation, CENPB forms a homodimer and interacts directly with CENP-A and CENP-C to facilitate CENP-A deposition and CENP-C recruitment for kinetochore assembly. It also associates with histone H3 and contributes to centromeric heterochromatin maintenance. Downstream, CENPB promotes assembly of the KMN network (KNL1, Mis12 complex, Ndc80 complex) essential for microtubule attachment and chromosome segregation. CENPB disruption thus impairs kinetochore assembly, causing defective chromosome congression, mitotic arrest, and chromosomal instability.
In Raji B cells, CENPB knockout is significant for modeling chromosomal instability in lymphoma. CENPB loss is predicted to induce aneuploidy and aberrant mitosis, hallmarks of Burkitt lymphoma. CENPB is also an autoantigen in systemic sclerosis, enabling study of autoimmune centromere responses. The combination of CENPB knockout with EBV-driven proliferation offers a platform to explore centromere dysfunction, genomic instability, and B-cell malignancy, and to screen for anti-centromere antibodies.
This polyclonal knockout population supports diverse experiments. Western blotting confirms CENPB deletion; immunofluorescence visualizes kinetochore mislocalization; flow cytometry analyzes cell cycle and mitotic indices. Karyotyping and comet assays assess chromosomal abnormalities and DNA damage, and proliferation assays reveal growth defects. Applications include centromere assembly studies, chromosomal instability pathways in lymphoma, and anti-centromere autoantibody assays. For more details, please contact Ascent Research.
