PBRM1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line. This polyclonal pool contains a heterogeneous mix of cells carrying CRISPR-mediated disruptions in the PBRM1 gene, providing a loss-of-function model for studying PBRM1-dependent processes. The use of polyclonal knockout cells enables robust, population-level analyses while mitigating clonal variation. The PBRM1 gene encodes BAF180, a core subunit of the PBAF SWI/SNF chromatin remodeling complex, and its disruption in a lymphoma context is particularly relevant for investigating tumor suppression and epigenetic regulation.
Raji cells are an EBV-positive Burkitt’s lymphoma-derived B lymphoblastoid cell line, widely used as a model for B-lymphocyte biology and lymphomagenesis. They exhibit constitutive activation of survival and proliferation signals, making them a valuable system for examining oncogenic mechanisms. The lymphoblastoid nature of Raji cells supports studies of B cell receptor signaling, transcriptional regulation, and viral oncogenesis. Importantly, Raji cells possess an intact DNA damage response and interferon signaling pathways, which are directly relevant to PBRM1 function.
PBRM1 (BAF180) is essential for PBAF complex-mediated chromatin remodeling, facilitating nucleosome repositioning to regulate gene expression. It functions downstream of ATM and ATR kinases in the DNA damage response, promoting p53-dependent transcription of target genes such as CDKN1A (p21). Additionally, PBRM1 interfaces with STAT1 and interferon-alpha signaling, modulating the expression of interferon-stimulated genes (ISGs) like IFIT1 and ISG15. PBRM1 interacts with ARID2, BRD7, SMARCC1, and SMARCD1 within the SWI/SNF complex, and its loss disrupts chromatin accessibility at regulatory regions, impairing DNA repair, cell cycle arrest, and immune responses.
In Raji B lymphocytes, PBRM1 knockout can reveal its tumor-suppressive roles within a lymphoid environment. Given that Raji cells are derived from Burkitt’s lymphoma, where MYC deregulation drives proliferation, the PBRM1 disruption may cooperate with MYC to promote oncogenesis by further compromising genomic stability and apoptotic checkpoints. This model is particularly suited to dissect the interplay between chromatin remodeling and oncogenic signaling in B-cell malignancies, and to evaluate how PBRM1 loss sensitizes cells to DNA-damaging agents or immunomodulatory drugs.
Researchers can use these polyclonal knockout cells in a variety of functional assays, including Western blotting for BAF180 to confirm knockout, RT-qPCR for ISG induction, ChIP-qPCR to assess chromatin changes, and ??H2AX immunofluorescence to monitor DNA damage. Flow cytometry enables cell cycle and apoptosis profiling, while RNA-seq provides transcriptome-wide insights. This model facilitates drug sensitivity screening, particularly for agents targeting the SWI/SNF complex or DNA repair pathways. For further technical details or custom inquiries, please contact Ascent Research.
