The NCOA3 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji human B lymphocyte line, designed to disrupt the NCOA3 gene and create a loss-of-function model for investigating transcriptional coactivation mechanisms in B-cell biology and oncogenic signaling. This product provides a heterogeneous pool of knockout cells, enabling functional studies of NCOA3 in the context of Burkitt lymphoma-derived lymphoblastoid cells without isolation of individual clones.
The Raji cell line is an Epstein-Barr virus (EBV)-positive lymphoblastoid line established from a Burkitt lymphoma patient. These human B lymphocytes serve as a well-characterized model for B-cell lymphoma research, immune response studies, and antigen-presenting cell investigations. The EBV-transformed background contributes to altered signaling networks and constitutive activation of specific transcriptional programs, making Raji cells particularly valuable for dissecting oncogenic pathways in lymphoid malignancies.
NCOA3, also designated SRC-3 or AIB1, is a transcriptional coactivator that potentiates the activity of nuclear receptors such as estrogen receptor ?? (ESR1), progesterone receptor, and androgen receptor, as well as other transcription factors including AP-1 and NF-??B. Through interactions with coactivators like CBP/p300 and protein arginine methyltransferase CARM1, NCOA3 enhances the expression of target genes critical for cell proliferation and survival. Upstream signals from estrogen, androgen, EGFR/HER2, PI3K/AKT, and MAPK pathways converge on NCOA3, while downstream effectors include CCND1 (cyclin D1), MYC, BCL2, HER2/ERBB2, MMP9, and BIRC5 (survivin). Dysregulation of NCOA3 promotes oncogenic transformation via constitutive activation of hormone and growth factor signaling cascades.
In the Raji B-cell context, NCOA3 knockout provides a system to explore coactivator functions independent of steroid hormone signaling, focusing on transcriptional networks central to B-cell lymphomas. NCOA3 is implicated in NF-??B and AP-1 pathways commonly hijacked in lymphoid malignancies, and its loss may alter expression of proliferation and anti-apoptotic genes, offering insights into lymphoma biology. This model is particularly relevant for studying cross-talk between cytokine signaling and transcriptional regulation, as well as mechanisms of drug resistance in B-cell cancers.
Researchers can employ this polyclonal knockout model in diverse functional assays, including Western blotting and RT-qPCR to confirm target disruption and assess downstream gene expression, RNA-seq for transcriptomic profiling, flow cytometry to monitor apoptosis and proliferation, reporter gene assays to measure transcriptional activity, co-immunoprecipitation to probe interactomes, ChIP-qPCR for chromatin occupancy, and drug sensitivity assays such as MTT or CellTiter-Glo. Specific applications encompass studying NCOA3’s contribution to B-cell lymphomagenesis, investigating NF-??B-driven transcriptional programs, evaluating hormone-independent coactivator roles in immune cells, and performing cancer drug sensitivity or resistance studies. For additional details, contact Ascent Research.
