The NCOA2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the NCOA2 gene is disrupted in Raji B lymphoblastoid cells. This mixture of edited cells provides a loss-of-function model to study coactivator biology without clonal selection bias, suitable for functional genomics and drug target evaluation.
Raji is an Epstein-Barr virus-positive Burkitt lymphoma cell line, widely used as a model for B cell malignancies and immune signaling. These B lymphocytes exhibit constitutive NF-??B and MYC activity, reflecting key oncogenic pathways. Their robust growth and ease of genetic manipulation make them ideal for investigating lymphoma-driving genes.
NCOA2 is a p160 transcriptional coactivator that links nuclear receptors and transcription factors to basal machinery. It is activated by estrogen receptor, glucocorticoid receptor, and thyroid hormone receptor, and interacts with MYC, STAT3, and CBP/p300. Downstream targets include CCND1, BCL2, MYC, and SLC2A1, driving proliferation and survival. In B cells, NCOA2 integrates B cell receptor?CBTK?CNF-??B signaling to promote gene expression.
In Raji cells, NCOA2 supports oncogenic programs mediated by MYC and NF-??B. Its disruption likely impairs expression of CCND1 and BCL2, reducing proliferation and sensitizing cells to apoptosis. The model thus reveals coactivator dependencies in aggressive lymphoma and allows examination of cross-talk among hormone, growth factor, and immune signaling pathways converging on NCOA2.
Applications include transcriptomic profiling by RNA-seq, chromatin occupancy analysis via ChIP-qPCR, and functional assays such as proliferation/apoptosis and MYC reporter assays. The cells facilitate studies of nuclear receptor coactivator roles in hematopoietic cancers and preclinical testing of coactivator-targeting agents. For further information, please contact Ascent Research.