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Cat. No. ARG1074

CHD2 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The CHD2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited human B lymphoblastoid cell population with disrupted CHD2 gene function. Derived from the Raji B-cell lymphoma line, these polyclonal knockout cells provide a physiologically relevant model for studying the ATP-dependent chromatin remodeler CHD2 in Notch signaling and chromatin dynamics. CHD2 is recruited by the RBPJ/NOTCH1-MAML1 complex to activate target genes such as HES1 and MYC. Loss of CHD2 impairs Notch-mediated transcription, making this model ideal for investigating Notch pathway regulation, B-cell lymphoma biology, and chromatin remodeling. Applications include ChIP, RNA-seq, proliferation assays, and drug screening.

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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

    CHD2

    Gene Identifier

    NCBI Gene ID 1106

    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 CHD2 Knockout Raji Polyclonal Cells are a human B-lymphocyte-based loss-of-function model generated by CRISPR/Cas9-mediated disruption of the CHD2 gene. This polyclonal knockout cell population preserves the parental Raji cell background while introducing heterogeneous target-gene mutations, enabling robust functional studies without the need for single-cell cloning.

The parental Raji cell line, derived from a Burkitt’s lymphoma patient, is an Epstein-Barr virus (EBV)-positive B lymphoblastoid line that grows in suspension. Raji cells retain key features of mature B lymphocytes, including surface immunoglobulin expression and antigen presentation capacity, and are widely utilized as a model for B-cell biology, lymphoma pathophysiology, and immune signaling research.

CHD2 is an ATP-dependent chromatin remodeler that functions as a transcriptional coactivator in the Notch signaling pathway. Following Notch activation, the NOTCH1 intracellular domain forms a complex with RBPJ and MAML1, which recruits CHD2 to Notch target gene promoters. CHD2 remodels nucleosomes to activate transcription of downstream effectors such as HES1, HEY1, MYC, and CCND1. It also interacts with histone chaperones SSRP1, SUPT16H, and the histone variant H3F3A, and participates in DNA damage repair pathways involving ATM/ATR. Thus, CHD2 integrates chromatin dynamics with gene expression and genome maintenance.

In the Raji lymphoma context, CHD2 disruption allows dissection of chromatin-dependent regulation of Notch target genes that drive proliferation and survival. Given the role of aberrant Notch signaling in B-cell malignancies, this knockout model enables investigation of CHD2’s contribution to oncogenic transcriptional networks and drug sensitivity. Additionally, it provides a platform to explore molecular parallels between CHD2-related neurodevelopmental disorders and cancer, leveraging the lymphoblastoid background for mechanistic studies.

The polyclonal knockout cells are suitable for diverse applications including Notch reporter assays, chromatin immunoprecipitation (ChIP)-qPCR, co-immunoprecipitation, and immunoblotting to probe CHD2 interactions and target regulation. Transcriptomic analyses (RNA-seq, RT-qPCR), proliferation, apoptosis, and drug sensitivity assays enable functional and pharmacological profiling. Flow cytometry can monitor B-cell surface markers. These cells support drug discovery targeting Notch or chromatin remodelers, and fundamental studies in epigenetics and lymphoma biology. For further information, please contact Ascent Research.

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