The EP300 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the EP300 gene has been disrupted in the Raji B-lymphocyte host background. This product provides a heterogeneous pool of cells carrying targeted gene modifications, enabling robust loss-of-function studies without the clonal selection artifacts associated with single-cell-derived lines. The polyclonal format maintains genetic diversity, reflecting more physiologically relevant population-level responses for downstream functional assays.
The Raji cell line is an Epstein-Barr virus (EBV)-positive lymphoblastoid B-cell line originally established from a Burkitt lymphoma patient. These cells are extensively employed as a model system for B-cell malignancies, apoptosis research, and immunoglobulin/immune signaling investigations. Raji cells exhibit hallmark features of Burkitt lymphoma, including rapid proliferation and dysregulated MYC expression, making them a relevant platform to dissect oncogenic mechanisms and evaluate therapeutic vulnerabilities in lymphoid cancers.
EP300 encodes the histone acetyltransferase p300, a transcriptional coactivator that acetylates histones H3 and H4 to relax chromatin, and directly acetylates p53 at lysine 382 and NF-??B p65 to enhance their transcriptional activity. p300 is regulated by upstream kinases including AKT, AMPK, cyclin-dependent kinases (CDK1/2), and DNA damage-responsive ATM/ATR, and integrates signals from mitogenic MAPK/ERK, TGF-??, and Hippo pathways. The coactivator forms complexes with CBP, PCAF, SMAD2/3, STAT3, YAP/TAZ, and nuclear receptors to fine-tune the expression of downstream targets such as CDKN1A (p21), BAX, and CCND1, thereby governing cell cycle progression, apoptosis, and differentiation.
Within the Raji B-cell lymphoma context, disruption of EP300 abrogates p300-dependent acetylation events, leading to defective p53-mediated tumor suppression and aberrant NF-??B-driven survival signaling. Loss of p300 coactivator function impairs the transcriptional activation of pro-apoptotic genes like BAX and the cell cycle inhibitor CDKN1A, while potentially altering the balance of pro-survival factors such as BCL2. Moreover, disrupted histone acetylation at key lymphoid gene promoters distorts B-cell receptor and JAK/STAT signaling networks central to lymphomagenesis. Consequently, these polyclonal knockout cells serve as a powerful model to interrogate how epigenetic dysregulation drives Burkitt lymphoma biology and to identify therapeutic vulnerabilities.
Researchers can employ the EP300 Knockout Raji Polyclonal Cells for Western blotting of acetyl-p53 (K382) and histone marks (H3K18ac, H3K27ac), RNA-seq transcriptome analysis, ChIP-qPCR of histone acetylation, and co-immunoprecipitation of p300 with p53 or NF-??B p65. The polyclonal population is suited for screening small-molecule p300 inhibitors or bromodomain modulators, testing drug sensitivity to agents such as etoposide and doxorubicin, and flow cytometry-based apoptosis (Annexin V/PI) and cell cycle assays. These applications enable detailed mechanistic studies of p300-dependent transcriptional regulation, epigenetic remodeling, and B-cell receptor signaling in lymphoma. For additional information, please contact Ascent Research.
