The DIP2A Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population in the Raji B lymphocyte line, enabling loss-of-function analyses of the DIP2A gene. This product offers a heterogeneous pool of edited cells for studying the consequences of DIP2A disruption in a lymphoma-relevant background, without requiring single-cell cloning. The polyclonal format captures diverse editing events, facilitating robust assessment of DIP2A-dependent phenotypes in a cellular context that retains key characteristics of Burkitt lymphoma.
The Raji cell line is an Epstein?CBarr virus (EBV)-positive B lymphocyte model derived from a Burkitt lymphoma patient. It is widely employed in immunology and cancer research due to its stable growth properties and relevance to B-cell malignancies. Raji cells express surface markers typical of mature B cells and are routinely used to study lymphocyte signaling, antibody production, and oncogenic transformation. The EBV-positive status further allows investigation of viral?Chost interactions and their impact on B-cell biology.
DIP2A encodes a protein that interacts directly with DNA methyltransferase 1 (DNMT1) and associates with the nucleosome remodeling and deacetylase (NuRD) complex, contributing to the maintenance of global DNA methylation patterns. Through its partnership with DNMT1, DIP2A participates in the transfer of methyl groups from S-adenosyl methionine to cytosine residues at CpG dinucleotides, thereby influencing the methylation landscape and downstream gene expression. Disruption of DIP2A can lead to DNA hypomethylation, altered chromatin structure, and dysregulation of genes involved in proliferation, differentiation, and neuronal development.
In the Raji cell background, DIP2A knockout provides a powerful tool for dissecting epigenetic mechanisms underlying B-cell lymphomagenesis. The EBV-positive nature of Raji cells adds a layer of complexity to DNA methylation regulation, making this model particularly suitable for exploring how DIP2A loss affects viral latency, host gene silencing, and malignant transformation. Researchers can examine the interplay between DIP2A-mediated methylation and B-cell differentiation programs, as well as the potential to reverse aberrant epigenetic marks in lymphoma.
Typical applications include bisulfite sequencing to assess genome-wide methylation changes, chromatin immunoprecipitation to evaluate DNMT1 and NuRD complex occupancy, and RT-qPCR to quantify expression of methylation-sensitive genes. Functional assays such as proliferation, apoptosis, and flow cytometry?Cbased phenotyping enable correlation of epigenetic shifts with cellular outcomes. This polyclonal knockout system supports mechanistic studies in cancer epigenetics, neurodevelopmental disorder modeling, and drug target validation. For additional information, please contact Ascent Research.
