The LRRC59 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line. This product provides a loss-of-function model for LRRC59, a gene encoding a nuclear envelope-associated protein, within a human Burkitt lymphoma background. The polyclonal format consists of a heterogeneous pool of cells carrying CRISPR/Cas9-mediated gene disruptions at the LRRC59 locus, avoiding clonal bias and reflecting a spectrum of editing outcomes. This resource is designed for researchers investigating the cellular functions of LRRC59 in a disease-relevant context, without the constraints of single-cell clonal expansion.
The Raji cell line is a suspension B lymphocyte line originally established from a Burkitt lymphoma patient. These cells maintain key characteristics of mature B cells, including the capacity for antibody production and antigen presentation, and serve as a workhorse model in immunological and cancer research. Raji cells proliferate rapidly and are readily transfectable, making them ideal for functional genomics and large-scale assays. Their B-cell origin is particularly relevant for studying lymphomagenesis, immune surveillance mechanisms, and the cell biology of lymphocyte activation.
The LRRC59 protein localizes to the nuclear envelope and plays a critical role in regulating nuclear envelope dynamics during mitosis. Mechanistically, LRRC59 interacts with nucleoporins NUP155 and NUP160 and with lamin A (LMNA) to coordinate nuclear pore complex organization and mitotic spindle assembly. It functions downstream of cell cycle regulatory kinases and nuclear envelope disassembly signals, and it is essential for accurate cell cycle progression. The broader molecular network includes components such as NUP155, NUP160, LMNB1, and CDK1, which participate in nuclear envelope and mitotic control. Disruption of LRRC59 leads to aberrant nuclear pore distribution and impaired mitotic progression, underscoring its importance in linking nuclear architecture to the cell division machinery.
In the Raji B lymphocyte context, knockout of LRRC59 disrupts nuclear envelope dynamics and mitotic fidelity, processes that are particularly vital for rapidly dividing lymphoma cells. Burkitt lymphoma is driven by deregulated proliferation, and defects in nuclear envelope assembly can compromise genomic stability and drug response. This model enables dissection of the dependency of B-cell malignancies on efficient mitotic progression and nuclear organization. It may uncover targetable vulnerabilities linked to LRRC59-mediated pathways, relevant to understanding both B-cell lymphoma and broader nuclear envelopathies.
These polyclonal knockout cells are applicable to a broad range of experimental workflows, including B-cell lymphoma modeling, nuclear envelope dynamics studies, mitotic regulation analysis, functional genomics screening, and drug sensitivity profiling. Researchers can assess LRRC59 protein loss by Western blotting, visualize nuclear envelope markers such as NUP155 and LMNA by immunofluorescence microscopy, perform cell cycle analysis by flow cytometry, measure proliferation, conduct live-cell imaging of mitosis, profile transcriptional changes by RNA-seq, and test drug sensitivity with agents like doxorubicin and vincristine. For further information or technical assistance, please contact Ascent Research.
