CIC Knockout Raji Polyclonal Cells are a polyclonal knockout cell population generated through CRISPR/Cas9-mediated gene disruption of the CIC locus in the Raji human B lymphocyte cell line. This polyclonal format comprises a heterogeneous pool of cells harboring CIC loss-of-function, enabling robust population-level analyses of CIC-dependent phenotypes without the clonal bias inherent to monoclonal lines. The product serves as a versatile tool for studying CIC??s regulatory roles in B-cell signaling and malignancy.
Raji is an Epstein-Barr virus-positive lymphoblastoid cell line derived from a Burkitt lymphoma patient, widely employed in immunological and oncological research. As a suspension B-cell line, it recapitulates key features of aggressive B-cell lymphoma and is a standard model for investigating B-cell receptor signaling, apoptosis, and oncogenic pathways including MAPK/ERK. Raji cells are particularly suited for studying mechanisms that drive lymphomagenesis and for screening therapeutic agents targeting B-cell malignancies.
CIC functions as a transcriptional repressor that targets ETS-family oncogenes such as ETV1, ETV4, and ETV5. Under basal conditions, CIC assembles repressive complexes with ATXN1, ATXN1L, SIN3A, and HDAC1 to silence these loci. Upon receptor tyrosine kinase stimulation by growth factors (e.g., EGF, FGF), the RAS-MEK-ERK signaling cascade phosphorylates CIC, triggering 14-3-3 protein binding, nuclear export, and proteasomal degradation. This relieves repression of ETV transcription factors, which then promote expression of genes like CCND1, MMP1, and MMP3, effectors of cell proliferation and survival. Thus, CIC operates as a key node linking extracellular cues to transcriptional output via the RTK-RAS-ERK axis.
In the Raji B-lymphoma context, CIC disruption generates a loss-of-function model to interrogate how derepression of ETS-family genes contributes to B-cell transformation and drug responses. Given the centrality of MAPK signaling in lymphocyte biology, this knockout population allows direct assessment of CIC??s impact on proliferation, apoptosis, and sensitivity to pathway inhibitors such as MEK inhibitors. The model is particularly valuable for studying the interplay between CIC status and ERK activity in a malignant B-cell background, and for identifying synthetic lethal interactions with CIC deficiency.
Researchers can employ this polyclonal knockout population for a range of applications, including functional dissection of MAPK/ERK-dependent transcription, drug sensitivity screening, and genome-wide expression profiling. Typical assays include western blot detection of CIC and ETV4, RT-qPCR quantification of ETV1/4/5 transcripts, phospho-ERK flow cytometry, cell viability assays (MTT), and apoptosis assessment by Annexin V/PI staining. RNA-sequencing enables global identification of CIC-regulated networks. For customization and additional information, please contact Ascent Research.
