The GATAD2B Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-engineered polyclonal knockout population of the Raji human B lymphocyte line, in which the GATAD2B gene has been disrupted to create a loss-of-function model. The polyclonal format provides a heterogeneous pool of edited cells, minimizing the impact of clonal variation and enabling robust assessment of gene function in pooled assays. This product is suitable for investigating the role of the NuRD complex without the need for single-cell cloning.
Raji is a B lymphocyte cell line derived from a Burkitt’s lymphoma patient, characterized by its rapid proliferation and expression of B cell markers. It serves as a well-established model for B cell biology, including studies of immunoglobulin production, immune signaling, and oncogenic transformation. The Raji system is particularly valuable for dissecting transcriptional regulation in the context of lymphoid malignancies, as it retains key B cell regulatory networks.
GATAD2B is a core component of the nucleosome remodeling and deacetylase (NuRD) complex, a multisubunit assembly that couples ATP-dependent chromatin remodeling with histone deacetylation to enforce transcriptional repression. Within the complex, GATAD2B interacts with CHD4 (chromodomain helicase DNA binding protein 4), histone deacetylases HDAC1 and HDAC2, metastasis-associated protein MTA1, methyl-CpG binding domain protein MBD2, and retinoblastoma binding protein RBBP4. Together, these factors silence target genes critical for development and differentiation. Disruption of GATAD2B impairs NuRD activity, leading to derepression of downstream targets and aberrant chromatin states. Mutations in GATAD2B are directly implicated in GAND syndrome, a neurodevelopmental disorder presenting with intellectual disability, highlighting its importance in neurological function. Upstream regulation of GATAD2B involves transcriptional and epigenetic mechanisms that modulate its expression and activity.
In the Raji B cell model, GATAD2B knockout enables the study of NuRD-dependent transcriptional control in a lymphoid environment. The NuRD complex has been shown to orchestrate gene programs governing B cell development, differentiation, and homeostasis, and its dysregulation is associated with lymphomagenesis. By ablating GATAD2B, researchers can interrogate how loss of this subunit alters chromatin accessibility and gene expression patterns in B cells, potentially identifying new targets and pathways involved in B cell transformation. This polyclonal knockout pool offers a physiologically relevant system to explore the intersection of chromatin remodeling and immune cell biology.
This product is designed for advanced functional genomics applications, including NuRD complex characterization, chromatin remodeling studies, and modeling of neurodevelopmental disorders such as GAND syndrome. Researchers can employ standard techniques such as Western blotting for protein expression verification, RT-qPCR for transcriptional profiling of target genes, ChIP-qPCR for histone modification and complex binding analyses, and RNA-seq for comprehensive transcriptomic insights. Proliferation assays can assess the impact of GATAD2B loss on Raji cell growth dynamics. For additional technical support, please contact Ascent Research.
