CDKN1C Knockout Raji Polyclonal Cells constitute a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population in which the CDKN1C gene has been disrupted. This product provides a heterogeneous pool of Raji-derived cells carrying a spectrum of targeted-gene disruptions, enabling direct analysis of CDKN1C loss-of-function phenotypes without clonal isolation. The polyclonal format preserves population-level diversity, facilitating robust statistical comparisons and minimizing clonal artifacts, making it well-suited for routine cell-cycle studies, apoptosis profiling, and drug-response evaluations.
The parental Raji cell line is a suspension-adapted human B-lymphoblastoid line established from a Burkitt??s lymphoma patient and immortalized by Epstein??C?Barr virus (EBV) transformation. Raji cells retain key characteristics of mature B lymphocytes, including surface immunoglobulin expression, antigen-presentation capability, and active antibody production. Their well-characterized chromosomal translocations and rapid growth kinetics have made them a workhorse model for investigating B-cell malignancies, immune signaling, and lymphomagenesis. The availability of this knockout panel in a suspension background simplifies culture handling and allows seamless integration into high-throughput screening workflows.
At the molecular level, CDKN1C encodes p57Kip2, a broad-specificity cyclin-dependent kinase (CDK) inhibitor that enforces G1-phase arrest by binding and inhibiting CDK2/cyclin?E and CDK4/cyclin?D complexes. This inhibition maintains retinoblastoma protein (RB1) in a hypophosphorylated state, preventing E2F-mediated transcriptional activation of S-phase genes. CDKN1C independently blocks replication elongation through direct interaction with proliferating cell nuclear antigen (PCNA). In parallel, it promotes apoptosis via LIMK1 regulation. The gene is transcriptionally activated by TGF???, glucocorticoids, p53, and FOXO transcription factors, and it suppresses expression of downstream effectors such as MYC, cyclin?D, and cyclin?E, positioning it centrally within cell-cycle checkpoints and stress-response networks.
Loss of CDKN1C function in Raji cells recapitulates alterations frequently observed in Burkitt??s lymphoma and other MYC-driven malignancies, where p57Kip2 silencing contributes to unchecked G1?to?S progression and survival under genotoxic stress. This knockout model therefore provides a disease-relevant cellular context for examining how glucocorticoid or TGF??? signaling converges on the cell-cycle machinery. It also offers a platform for exploring mechanisms underlying Beckwith?CWiedemann syndrome and IMAGe syndrome, conditions linked to CDKN1C mutations.
Typical research applications include dissecting cell-cycle dysregulation in lymphomagenesis, evaluating glucocorticoid-induced apoptosis and drug resistance, and mapping CDKN1C-dependent signaling pathways. Representative assays supported by this model are flow-cytometric cell-cycle analysis (propidium iodide staining), Western blotting for CDKN1C and downstream targets, RT?qPCR quantification of target-gene expression, co-immunoprecipitation to assess CDK or PCNA interactions, proliferation assays (MTT or BrdU), Annexin?V apoptosis detection, and dexamethasone or chemotherapeutic sensitivity profiling. For further details, please contact Ascent Research.
