LSM14B Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from Raji B lymphocytes, featuring disruption of the LSM14B gene. This loss-of-function model enables investigation of LSM14B-mediated post-transcriptional regulation in a human B-cell context.
The Raji cell line, established from a Burkitt’s lymphoma patient, is a widely used model of B-cell biology and lymphoma. These suspension cells retain mature B-cell functions, including surface immunoglobulin expression and antigen presentation, and provide a robust system for studying RNA metabolism, signaling pathways, and cell proliferation.
LSM14B (RAP55B) is a scaffold protein essential for processing bodies (P-bodies), where it orchestrates mRNA decapping and 5??C3?? decay. It associates with the decapping complex comprising DCP1a and DCP2, the exonuclease XRN1, and the LSM1-7 heptameric ring, facilitating cap removal and transcript degradation. Additionally, LSM14B interacts with PATL1, DDX6, and LSm14A to coordinate translational repression and mRNA storage. Upstream, its activity is modulated by stress signaling and microRNAs, while downstream it controls the stability of target mRNAs implicated in cell cycle progression, apoptosis, and immune responses. This positions LSM14B as a central post-transcriptional regulator in B lymphocytes.
In the Raji B-cell model, loss of LSM14B disrupts P-body integrity and decapping-dependent mRNA decay, thereby altering the post-transcriptional regulation of transcripts critical for lymphomagenesis and immune function. This perturbation is expected to stabilize pro-proliferative and anti-apoptotic mRNAs, potentially enhancing oncogenic pathways, while also dysregulating mRNAs encoding cytokines and surface receptors involved in antigen presentation. Consequently, the knockout model offers a unique platform to dissect how P-body-mediated mRNA control influences B-cell homeostasis and transformation.
These polyclonal knockout cells are suitable for a variety of functional studies, including immunofluorescence staining of P-bodies, RNA immunoprecipitation (RIP) to map LSM14B target transcripts, and metabolic labeling or actinomycin D chase assays to quantify mRNA decay kinetics. Proliferation assays and flow cytometry can be employed to evaluate the impact of LSM14B loss on B-cell growth and survival. The model is particularly advantageous for investigating aberrant RNA regulation in Burkitt’s lymphoma and for screening potential therapeutic compounds that target the mRNA decay machinery. For further information, please contact Ascent Research.
