The PAN3 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human Raji B lymphocyte cell line, targeting the PAN3 gene (Homo sapiens) for loss-of-function analysis. This heterogeneous pool of edited cells harbors targeted disruption of the PAN3 locus via CRISPR/Cas9-mediated gene disruption, offering a robust model to study PAN3-dependent mRNA deadenylation and its impact on post-transcriptional gene regulation without clonal selection.
Raji cells are a human B lymphocyte model derived from a Burkitt lymphoma, an aggressive B-cell malignancy. They exhibit lymphoblastoid morphology and retain key features of humoral immunity, including surface immunoglobulin expression. Widely utilized in immunology and oncology, Raji cells provide a well-characterized system for investigating lymphoma biology, antigen presentation, and the regulation of mRNA metabolism. Their rapid proliferation and amenability to genetic manipulation facilitate functional genomics studies.
PAN3 encodes the regulatory subunit of the PAN2-PAN3 cytoplasmic deadenylase complex, which shortens poly(A) tails on target mRNAs to promote mRNA decay, a central mechanism in the mRNA surveillance pathway and deadenylation-dependent mRNA decay. Upstream, argonaute proteins and miRNA-mediated deadenylation regulate PAN2-PAN3 activity, directing the complex to specific transcripts. The complex interacts with the catalytic subunit PAN2, and its downstream targets are poly(A)-containing mRNAs. Within the RNA degradation network, PAN3 cooperates with the CCR4-NOT deadenylase complex and poly(A)-binding protein (PABP). Knockout of PAN3 impairs deadenylation, stabilizing polyadenylated transcripts and altering gene expression.
In the Raji background, PAN3 knockout is particularly significant given the association between aberrant mRNA turnover and Burkitt lymphoma pathogenesis. Dysregulation of deadenylation can disrupt oncogene and tumor suppressor expression, contributing to lymphomagenesis. This model allows dissection of how mRNA stability influences B lymphocyte proliferation, differentiation, and transformation. The polyclonal nature captures population-level edit diversity, enabling bulk mRNA decay analyses that reflect heterogeneous tumor environments and facilitating the study of global post-transcriptional control in lymphoma.
These knockout cells support diverse applications, including post-transcriptional gene regulation studies, mRNA stability analysis, and nonsense-mediated decay investigations. They are compatible with RT-qPCR, RNA-seq, mRNA half-life measurements, luciferase reporter assays, and polysome profiling. Such approaches enable characterization of PAN3-dependent pathways in B cell malignancies and identification of therapeutic targets. For further information, please contact Ascent Research.
