The PCGF6 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the PCGF6 gene in the Raji B-cell line. This product provides a heterogeneous pool of edited cells, enabling researchers to study the loss-of-function effects of PCGF6 in a physiologically relevant malignant B-cell context. By ablating PCGF6 expression across a mixed population, the model captures diverse genetic backgrounds arising from the editing process, offering a robust system for functional genomics and epigenetic investigations.
The Raji cell line is a suspension-growing lymphoblastoid line derived from a Burkitt lymphoma patient, an 11-year-old Nigerian boy. These cells are Epstein-Barr virus (EBV) positive and retain characteristic malignant B-cell features, including aberrant proliferation and survival signaling. Raji cells serve as a widely adopted model for B-cell biology, EBV latency, and lymphoma research, providing a consistent and well-characterized host for studying oncogenic mechanisms and epigenetic regulation in hematopoietic malignancies.
PCGF6 encodes a polycomb group RING finger protein that functions as a core subunit of the non-canonical PRC1.6 complex. Within this complex, PCGF6 collaborates with RING1A and RING1B to catalyze monoubiquitination of histone H2A at lysine 119 (H2AK119ub), a chromatin mark associated with transcriptional silencing. PCGF6 interacts with L3MBTL2, CBX3 (HP1??), and KDM2B to target specific genomic loci, including HOXA and HOXB cluster genes, CDKN2A/p16, and CDKN2B/p15. Its activity is regulated by upstream factors such as MYC, E2F transcription factors, and the EBV latent membrane protein LMP1, linking polycomb silencing to lymphoma-driving pathways.
In the Raji B-cell context, PCGF6-mediated repression is critical for maintaining the expression programs that govern proliferation, differentiation, and oncogenic transformation. Disruption of PCGF6 abrogates PRC1.6 complex function, leading to reduced H2AK119ub deposition at target genes and derepression of tumor suppressor loci such as CDKN2A and CDKN2B. This perturbation can impair B-cell growth and survival, while also modulating EBV latency programs influenced by LMP1 and host transcription factors. Consequently, this knockout model enables dissection of polycomb-dependent epigenetic mechanisms underlying Burkitt lymphoma pathogenesis and the interplay between viral oncoproteins and host chromatin regulation.
Researchers can employ PCGF6 Knockout Raji Polyclonal Cells in a broad array of experimental applications, including chromatin immunoprecipitation (ChIP-qPCR) to assess H2AK119ub and PRC1 subunit occupancy, RNA sequencing to profile transcriptomic changes, western blotting for PCGF6 and associated complex members, and flow cytometry to monitor B-cell surface marker expression. Functional assays such as cell proliferation (MTT, CellTiter-Glo) and apoptosis (Annexin V) further support drug screening and target validation studies aimed at the PRC1.6 complex or upstream regulators like MYC and E2F. For more information on integrating this model into your research, please contact Ascent Research.
