The ESRRA Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal Raji cell population with targeted disruption of the ESRRA gene, encoding the orphan nuclear receptor ERR??. This polyclonal pool offers a flexible loss-of-function model for studying ERR??-mediated transcriptional and metabolic regulation without clonal selection, enabling analysis of gene function in a heterogeneous lymphoma cell context.
Raji is an Epstein-Barr virus (EBV)-positive human Burkitt lymphoma B lymphoblastoid cell line widely used as a model for B-cell biology, lymphoma pathogenesis, and immune signaling. Raji cells grow in suspension and express characteristic B-cell markers, facilitating standard cell culture and flow cytometry-based experimentation. The line retains key features of transformed B lymphocytes, including constitutive activation of survival pathways and reliance on glycolytic and mitochondrial metabolism for rapid proliferation. Its EBV-positive status also makes it relevant for studying viral manipulation of host cell metabolism.
ESRRA encodes a nuclear receptor that, upon coactivation by PPARGC1A (PGC-1??), binds estrogen-related response elements to drive genes involved in mitochondrial biogenesis, fatty acid oxidation, and oxidative phosphorylation. Upstream energy sensors AMPK and SIRT1 converge on ESRRA regulation, modulating its activity in response to ATP depletion. Key transcriptional targets include ATP5B, COX5B, and CYCS for respiratory chain function, and PDK4 and CPT1B control metabolic substrate utilization. ERR?? activity is further modulated by corepressor NRIP1 (RIP140) and coactivators NCOA1/SRC-1 and NCOA2/GRIP1, which together dictate transcriptional output.
In Raji cells, ESRRA knockout disrupts the PGC-1??/ERR?? signaling node, impairing mitochondrial respiration and metabolic flexibility critical for lymphoma cell growth and survival. This model enables dissection of ERR????s role in coupling energy metabolism to B-cell receptor and survival signaling, and facilitates identification of metabolic vulnerabilities that may be therapeutically targeted in Burkitt lymphoma.
Applications include investigating ERR??-driven metabolic reprogramming in lymphoma, validating ERR?? as a candidate drug target, and examining mitochondrial biogenesis in B-cell malignancies. Compatible assays comprise Western blotting and RT-qPCR for target gene expression, genomic DNA sequencing for knockout verification, flow cytometry for cell cycle and apoptosis analysis, Seahorse metabolic flux profiling, and functional assays such as proliferation, migration, and invasion. For technical support or further details, please contact Ascent Research.
