The LRRCC1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the LRRCC1 gene in the Raji B lymphocyte host. This product provides a loss-of-function model for investigating LRRCC1-dependent processes in a suspension-adapted, Epstein-Barr virus (EBV)-transformed lymphoblastoid cell line. The polyclonal nature of the knockout population ensures representation of diverse editing outcomes, enabling robust functional studies without clonal bias.
Raji cells, originally derived from a Burkitt’s lymphoma patient, are a widely used human B lymphocyte line that maintains key immunological characteristics including surface expression of CD19 and CD20. These cells grow in suspension and are permissive for studies of antibody production, antigen presentation, and immune surveillance. Their EBV-transformed status provides a stable, continuously proliferating background that complements the knockout phenotype by allowing examination of centrosome-associated mechanisms within a B cell malignancy context.
LRRCC1 encodes a centrosomal protein essential for centriole elongation and proper ciliogenesis, thereby contributing to cell cycle progression. Mechanistically, LRRCC1 localizes to the centrosome and facilitates centriole elongation through direct interaction with CEP135. Its function is regulated by upstream kinases including PLK4, Aurora A kinase, and CDK2, and it acts downstream of these regulators to influence assembly of centriolar components such as SAS-6 and CPAP. The LRRCC1-containing centrosome duplication pathway further integrates signals from STIL and CEP120, coordinating centriole biogenesis with cell cycle transitions.
In the Raji B lymphocyte system, LRRCC1 knockout provides a pertinent model to dissect centrosome biology within a lymphoid malignancy background. Aberrant centriole numbers and centrosome amplification are hallmarks of many cancers, including Burkitt’s lymphoma, and LRRCC1 disruption may reveal vulnerabilities associated with defective ciliogenesis or altered cell cycle control. This polyclonal population therefore enables the study of how loss of LRRCC1 impacts proliferation, apoptosis, and centrosome integrity in a cell type relevant to both ciliopathy research and B cell cancer biology.
Researchers can employ this knockout model in a variety of experimental workflows, including Western blotting to confirm LRRCC1 deficiency, immunofluorescence microscopy for centriolar markers such as ??-tubulin and CEP135, and flow cytometry to assess cell cycle perturbations. Further applications include RT-qPCR for transcriptional analysis, co-immunoprecipitation to probe CEP135 interactions, and functional assays like BrdU/MTT proliferation measurements or Annexin V apoptosis detection. These approaches facilitate detailed investigations into centrosome duplication, ciliogenesis, and B cell malignancy. For additional information or technical support, please contact Ascent Research.
