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.