The CSTF2 Knockout Raji Polyclonal Cells product comprises a population of Raji B lymphocytes engineered via CRISPR/Cas9-mediated gene disruption to eliminate functional expression of the CSTF2 gene. This polyclonal knockout pool, generated without single-cell cloning, enables researchers to interrogate the collective effects of CSTF2 loss on mRNA processing and B-cell biology. The heterogeneous nature of the population provides a robust model for studying gene function in a cellular context that retains the polyclonal diversity of the original Raji line, facilitating experiments that require population-level responses.
Raji cells, established from a patient with Burkitt??s lymphoma, are an Epstein-Barr virus (EBV)-positive B lymphocyte line with well-characterized properties in humoral immunity, including antigen presentation and antibody production. Their transformed phenotype and rapid proliferation make them a standard model for lymphomagenesis and B-cell malignancies. The cell line??s stable growth and amenability to genetic manipulation support detailed mechanistic studies of RNA processing and oncogenic signaling in a B-cell environment.
CSTF2 encodes a subunit of the cleavage stimulation factor (CstF) complex, which along with CSTF1 and CSTF3, recognizes GU-rich downstream elements in pre-mRNAs to direct 3′ end cleavage and polyadenylation. CSTF2 interacts with the CPSF complex (CPSF1?C4), symplekin, and RNA polymerase II to modulate alternative polyadenylation (APA) of transcripts including MYC and CCND1. The CstF complex functions downstream of the MYC transcription factor, which upregulates CSTF2 expression, and regulates poly(A) site choice, thereby influencing mRNA stability and translation. Disruption of CSTF2 impairs normal 3′ end processing, leading to widespread shifts in APA and altered gene expression profiles, particularly of proliferation-associated mRNAs.
In Raji cells, CSTF2 knockout disrupts the precise regulation of APA that is critical for B-cell proliferation and survival, potentially mimicking or counteracting mechanisms active in B-cell lymphoma. The loss of CSTF2-mediated processing of MYC and CCND1 transcripts may attenuate oncogenic signaling, making this model valuable for dissecting how APA contributes to lymphomagenesis. Coupled with the cells?? EBV-positive background, the knockout provides a tool to investigate virus?Chost interactions affecting RNA processing and immune function, revealing new dimensions of B-cell pathology.
This polyclonal knockout cell product is suited for a range of applications, from genome-wide alternative polyadenylation profiling using RNA-seq to targeted isoform analysis by 3′ RACE and qRT-PCR. Researchers can employ co-immunoprecipitation to assess residual CstF complex assembly or utilize flow cytometry and cell proliferation assays to link APA changes to phenotypic outcomes. The model also enables drug-sensitivity screens and validation of APA modulators in a lymphoma context. For additional information or custom requests, please contact Ascent Research.
