MORF4L2 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Raji B lymphocyte line, engineered to disrupt the MORF4L2 gene. This loss-of-function model provides a powerful tool for investigating the biological roles of MORF4L2 in chromatin remodeling, transcriptional regulation, and DNA damage response within a relevant lymphoblastoid background. The polyclonal nature of the product ensures a heterogeneous pool of edited cells, reflecting a spectrum of knockout efficiencies that is particularly useful for studying heterozygous and population-level phenotypes without requiring single-cell cloning. As a research-grade reagent, these cells are designed for use in advanced biomedical investigations, including functional genomics, epigenetic profiling, and drug target validation.
Derived from a patient with Burkitt’s lymphoma, Raji cells are Epstein-Barr virus (EBV)-positive lymphoblastoid B lymphocytes that retain key features of antibody production and antigen presentation. This cell line is a well-established model for B-cell malignancies, offering a clinically relevant platform to study lymphomagenesis, immune surveillance, and the molecular underpinnings of hematopoietic cancers. The EBV-positive status and active transcriptional program of Raji cells make them particularly suitable for examining how chromatin-modifying complexes, such as the NuA4/TIP60 complex, influence gene expression and genome stability in a tumorigenic context.
MORF4L2 is a core subunit of the NuA4/TIP60 histone acetyltransferase complex, which catalyzes acetylation of histone H4 at lysine 16 (H4K16ac) and histone H2A, promoting chromatin relaxation and facilitating transcription factor access. This protein interacts with several key complex components, including EP400, TRRAP, RUVBL1, and the catalytic subunit KAT5 (TIP60), and operates downstream of DNA damage signals mediated by ATM and ATR kinases. Functionally, MORF4L2-dependent acetylation regulates the expression of downstream targets such as the cell cycle inhibitor p21/CDKN1A and multiple DNA repair genes, thereby linking epigenetic modifications to cell cycle control and genomic maintenance. Disruption of MORF4L2 impairs stimulus-induced H4K16ac deposition, compromising the activation of transcriptional programs essential for DNA repair and cellular senescence.
In the Raji B lymphocyte background, MORF4L2 knockout provides a highly relevant model to study the intersection of epigenetic regulation and B-cell malignancy. Loss of MORF4L2 function is anticipated to attenuate DNA damage-induced chromatin acetylation, leading to defective repair of double-strand breaks and accumulation of genomic instability??a hallmark of Burkitt’s lymphoma and other aggressive lymphomas. This model enables researchers to dissect the mechanistic contributions of the NuA4/TIP60 complex to lymphomagenesis, explore synthetic lethal interactions with chemotherapeutic agents, and evaluate how disrupted histone acetylation patterns influence oncogenic signaling and tumor suppressor networks in EBV-positive B cells.
Typical research applications for these knockout cells encompass chromatin biology, DNA damage response studies, and lymphoma modeling. The cells are amenable to a variety of experimental techniques, including chromatin immunoprecipitation combined with quantitative PCR (ChIP-qPCR) to measure H4K16ac levels, RNA sequencing for transcriptome-wide analysis, co-immunoprecipitation to assess NuA4 complex integrity, flow cytometry for cell cycle profiling, and ??H2AX immunofluorescence to quantify DNA damage foci. Additionally, apoptosis assays and drug sensitivity screens can be performed to validate therapeutic targets. For detailed technical specifications and ordering information, please contact Ascent Research.
