The EID1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the EID1 gene, providing a loss-of-function model for studying EID1-dependent transcriptional regulation. This non-clonal pool preserves heterogeneous knockout genotypes, reducing clonal bias in functional experiments. The cells are delivered as a live culture ready for immediate use in downstream assays.
The Raji cell line originates from a Burkitt lymphoma patient and serves as an EBV-positive human B lymphocyte model. Raji cells retain characteristics of mature B cells, including roles in antigen presentation and antibody production, and are extensively employed in studies of B-cell malignancies and immune signaling.
EID1 functions as a transcriptional corepressor by directly binding to EP300 and CREBBP histone acetyltransferases and inhibiting their catalytic activity, thereby repressing E2F-mediated transcription. EID1 interacts with HDAC1, SIRT1, E2F1, and RB1 within multiprotein complexes that modulate chromatin structure. EID1 expression is regulated by upstream factors such as E2F1, MYC, p53, and retinoic acid. Its repressive activity targets E2F-responsive genes including CCNA2, CCNE1, and CDK1, while also influencing CDKN1A (p21). Thus, EID1 serves as a brake on cell cycle progression and differentiation, integrating signals from senescence and proliferation pathways.
In Raji B-lymphoma cells, knockout of EID1 is expected to relieve repression of E2F target genes, potentially accelerating cell cycle transit and modifying senescence programs. This model allows dissection of how loss of corepressor function contributes to lymphomagenesis, particularly in the context of EBV latency and cooperating oncogenic signals such as MYC overexpression. It also facilitates exploration of EID1??s role in retinoic acid and sirtuin signaling pathways within B lymphocytes.
The EID1 Knockout Raji Polyclonal Cells support a variety of applications: quantification of E2F target proteins (e.g., cyclin A, cyclin E) by Western blot and RT-qPCR, cell cycle analysis by flow cytometry, and senescence detection with SA-??-galactosidase. Transcriptome profiling via RNA-seq, protein interaction studies by co-immunoprecipitation of EP300, and EP300 HAT activity assays can elucidate mechanistic consequences. Proliferation assays (MTT) assess functional growth effects. For more information or to inquire about customized gene editing, please contact Ascent Research.
