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Cat. No. ARG1340

CDKN2A Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

These CDKN2A Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of EBV-positive human B lymphoblastoid cells with disruption of the CDKN2A tumor suppressor locus. Loss of the encoded p16INK4a and p14ARF proteins removes critical checkpoints in cell cycle control and apoptosis, relieving CDK4/6 inhibition and impairing p53-mediated tumor suppression. This model is ideal for cancer biology, cell cycle, and drug discovery studies, including assays for proliferation, apoptosis, and sensitivity to CDK4/6 or MDM2 inhibitors. It enables investigation of the p16INK4a/RB and p14ARF/p53 pathways and their roles in B-cell lymphomagenesis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Raji

    Cell Type

    B cell line

    Sex of Donor

    Male

    Age

    11 years

    Derived From Site

    In situ; Maxilla

    Gene Name

    CDKN2A

    Gene Identifier

    NCBI Gene ID 1029

    Morphology

    Lymphoblast-like

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The CDKN2A Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population generated from the Raji B lymphoblastoid cell line, with disruption of the CDKN2A tumor suppressor gene. This polyclonal format provides a heterogeneous pool of cells lacking p16INK4a and p14ARF expression, suitable for loss-of-function studies without clonal selection bias. The cells serve as a robust model for investigating CDKN2A-dependent cellular processes.

Raji is a suspension human B lymphoblastoid cell line established from a Burkitt lymphoma patient and is latently infected with Epstein?CBarr virus (EBV). This cell line is a well-established model for B-cell biology, lymphomagenesis, and immune responses, characterized by rapid proliferation and expression of B-cell markers. Its EBV-positive status and p53 wild-type background make it valuable for investigating oncogenic mechanisms and therapeutic interventions in B-cell malignancies.

CDKN2A encodes two tumor suppressors: p16INK4a, a CDK4/6 inhibitor that maintains RB1 in a hypophosphorylated state to repress E2F-mediated transcription and block G1/S transition, and p14ARF, which binds MDM2 to stabilize TP53 and enhance transcription of pro-apoptotic and cell cycle arrest genes such as CDKN1A and BAX. These pathways are activated by E2F1, RAS, and oncogenic stress, and are negatively regulated by BMI1. In knockout cells, loss of CDKN2A disrupts both the p16INK4a/RB and p14ARF/p53 signaling nodes.

Disruption of CDKN2A in Raji cells, which already harbor EBV-driven survival signals, accentuates proliferative capacity and resistance to apoptosis, mimicking the loss of tumor suppression seen in aggressive B-cell lymphomas and other CDKN2A-deficient cancers. This model enables dissection of cooperative mechanisms between viral oncoproteins and host tumor suppressors, and is relevant for testing interventions targeting CDK4/6 or MDM2.

This cell pool is suitable for Western blotting of CDKN2A proteins and downstream effectors, cell cycle profiling by flow cytometry, apoptosis assays, and proliferation measurements. It can be used in drug sensitivity screens with CDK4/6 inhibitors or MDM2 antagonists, as well as transcriptomic studies via RNA-seq or RT-qPCR. Applications include cancer biology, cell cycle regulation, senescence, and B-cell lymphoma research. For technical inquiries, contact Ascent Research.

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