The NR2C1 Knockout Raji Polyclonal Cells are a polyclonal knockout cell population produced by CRISPR/Cas9-mediated disruption of the NR2C1 gene in Raji cells. This product provides a heterogeneous pool of gene-edited cells, enabling functional studies of NR2C1 in a polyclonal B-lymphocyte background without clonal selection. The polyclonal format retains biological diversity while effectively abrogating NR2C1 expression, making it suitable for population-level analyses of orphan nuclear receptor function.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive B lymphoblastoid line derived from a Burkitt lymphoma patient. Raji cells serve as a well-characterized model for B-cell biology, humoral immunity, and oncogenic transformation. They express key B-cell surface markers and maintain active signaling networks relevant to lymphomagenesis, including NF-??B and MYC-driven pathways. This EBV-immortalized line proliferates robustly in suspension culture, facilitating reproducible experimental setups for gene perturbation studies.
NR2C1 (also known as TR2) is an orphan nuclear receptor that functions as a transcriptional repressor or activator depending on cellular context. It homodimerizes or heterodimerizes with the related receptor NR2C2 (TR4) or retinoid X receptor (RXR) to bind hormone response elements in target gene promoters. In the absence of known endogenous ligands, NR2C1 constitutively recruits co-repressors such as nuclear receptor co-repressor 1 (NCOR1) and silencing mediator for retinoid and thyroid hormone receptor (SMRT), or co-activators to modulate transcription. NR2C1 regulates genes involved in cell proliferation and differentiation, including the cell cycle inhibitor CDKN1A and steroidogenic enzyme CYP17A1. Signaling inputs include all-trans retinoic acid (ATRA), which may influence NR2C1 activity through RXR heterodimerization.
In Raji B cells, NR2C1 contributes to the transcriptional programs governing cell growth and survival. Disruption of NR2C1 in this lymphoma model is predicted to alter the expression of downstream targets and co-regulator interactions, impacting pathways relevant to lymphomagenesis. The polyclonal knockout population allows investigation of NR2C1??s role in B-cell proliferation, apoptosis, and differentiation without artifacts from clonal selection. This model provides a physiologically relevant context to assess how loss of NR2C1 affects Burkitt lymphoma cell behavior and response to therapeutic agents.
This polyclonal knockout population enables functional studies of NR2C1 in B-cell lymphoma, ligand screening for orphan nuclear receptors, and drug target validation. Typical assays include RT-qPCR and western blotting to verify NR2C1 disruption, cell proliferation (MTS/sulforhodamine B) and apoptosis (Annexin V) analyses, RNA-seq transcriptome profiling, ChIP-qPCR for NR2C1 binding sites, and luciferase reporter assays. The model supports drug sensitivity and co-culture studies. For further information, please contact Ascent Research.
