The DIS3L Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the DIS3L gene has been disrupted to abolish its functional expression. This product provides a ready-to-use cellular model for studying the catalytic subunit of the cytoplasmic RNA exosome in a human B lymphoblastoid background. The polyclonal format preserves the heterogeneity of the edited Raji cell pool, offering a robust tool for loss-of-function analyses without clonal selection bias. Researchers can utilize these cells to investigate DIS3L-dependent RNA decay mechanisms in a setting closely mimicking the native exosome environment.
Raji cells are a well-characterized human B lymphocyte line derived from a Burkitt lymphoma patient. They are Epstein-Barr virus (EBV)-positive and grow in suspension, retaining key features of transformed B cells. This makes them particularly suitable for immunological and cancer research, especially in the context of B-cell malignancies. The cell line??s genetic background includes known mutations and chromosomal translocations typical of Burkitt lymphoma, providing a disease-relevant platform for targeted gene knockout studies. Their robust proliferation and established handling protocols further enhance their utility for high-throughput and longitudinal assays.
DIS3L encodes a 3′-5′ exoribonuclease that functions as the catalytic subunit of the cytoplasmic RNA exosome complex, executing RNA surveillance and processing. It mediates the degradation of unstable mRNAs, aberrant transcripts, miRNAs, and other exosome substrates, thereby regulating gene expression and maintaining cellular RNA homeostasis. DIS3L acts downstream of upstream regulators including cell cycle-dependent expression cues, post-translational modifications, and exosome assembly factors, and its activity is modulated through interactions with core exosome subunits such as EXOSC10, EXOSC2, EXOSC3, and DIS3, as well as RNA helicases. The DIS3L-inclusive cytoplasmic exosome works in concert with pathway components such as the SKI complex, CCR4-NOT complex, and the 5′-3′ exonuclease XRN1 to coordinate RNA turnover. Disruption of DIS3L perturbs these networks, leading to accumulation of target RNAs and potential disruptions in gene expression programs.
In the Raji cell context, DIS3L knockout enables focused investigation of exosome-mediated RNA decay in B-cell malignancies. Burkitt lymphoma and other B-cell cancers often exhibit dysregulated RNA metabolism, and loss of DIS3L may exacerbate or illuminate pathways driving oncogenesis. The polyclonal knockout cells allow researchers to assess global effects on the transcriptome and proteome without clonal artifacts, providing insights into how exosome dysfunction contributes to lymphomagenesis. This model is particularly valuable for evaluating the consequences of RNA exosome inhibition on cell proliferation, apoptosis, and drug sensitivity, given the reliance of rapidly dividing lymphoma cells on efficient RNA processing.
These DIS3L knockout polyclonal Raji cells are suited for a range of advanced applications, including RNA decay assays, transcriptomic profiling via RNA-seq, and quantitative analysis of target mRNAs by RT-qPCR. Protein-level validation can be performed using western blotting, while co-immunoprecipitation enables mapping of altered exosome interactions. Functional studies may incorporate flow cytometry to monitor apoptotic and proliferative responses, as well as drug sensitivity screens to assess therapeutic targeting of RNA-processing enzymes. The model also supports mechanistic dissection of DIS3L-dependent pathways and identification of synthetic lethal interactions in B-cell lymphoma. For further information or technical inquiries, please contact Ascent Research.
