This product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ETV6 gene in the human Raji B-lymphocyte cell line. The polyclonal knockout pool offers a genetically heterogeneous loss-of-function model, enabling robust assessment of gene disruption effects without clonal selection bias. These cells are suitable for studying ETV6-dependent regulatory mechanisms in a hematopoietic context.
The Raji host cell line originates from a human Burkitt??s lymphoma and is characterized by its lymphoblastoid B-cell phenotype and Epstein-Barr virus (EBV) positivity. Raji cells are widely employed in immunological and oncological research due to their stable proliferation, well-documented signaling properties, and relevance to B-cell malignancies. Their EBV carrier status also provides a unique platform for exploring virus-host interactions.
ETV6 encodes an ETS family transcriptional repressor that recruits corepressor complexes including SMRT, N-CoR, mSin3A, and histone deacetylases (HDACs) to silence target genes. It functions downstream of SCF/KIT and IL-3 signaling, operating through JAK2/STAT5 and MAPK/ERK pathways. ETV6 directly represses transcription of genes such as MMP3 and BCL-XL and interacts with RUNX1 and FLI1. Its repressive activity is critical for normal hematopoiesis, angiogenesis, and cell differentiation, and its disruption is implicated in leukemogenesis via fusion proteins like ETV6-RUNX1.
In the Raji B-cell background, ETV6 knockout relieves transcriptional repression of genes involved in proliferation and survival, potentially altering B-cell differentiation programs. Given the EBV-positive status, the knockout may also modify virus-driven oncogenic pathways, making this model valuable for dissecting ETV6’s tumor-suppressive functions and interactions with latent viral proteins. This enables investigations into how ETV6 loss cooperates with EBV to perturb B-cell homeostasis.
These polyclonal knockout cells are suitable for a range of downstream applications, including RNA-seq and ChIP-qPCR for global gene expression and chromatin occupancy analysis, Western blotting for protein-level validation, and flow cytometry for phenotypic characterization. Proliferation and apoptosis assays can assess functional consequences of ETV6 disruption, while drug response studies may reveal synthetic lethal interactions. This model supports mechanistic research in B-cell malignancies, transcriptional repression, and EBV biology. For additional product details, technical support, or custom inquiries, please contact Ascent Research.
