The CGGBP1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B-lymphocyte line. This heterogeneous pool of cells with disrupted CGGBP1 enables robust loss-of-function studies without single-cell cloning artifacts. The polyclonal format maintains genetic diversity, supporting reproducible functional genomics and investigations of CGGBP1-dependent transcriptional regulation and CGG repeat biology in a B-cell context.
The Raji cell line is an Epstein-Barr virus (EBV)-positive, lymphoblastoid model of human Burkitt lymphoma. These B lymphocytes retain immune functions such as antigen presentation and are widely employed in immunology and oncology. EBV latency programs establish active transcriptional networks and oncogenic signaling, providing a distinct background to study gene function in transformed B-cell contexts.
CGGBP1 is a CGG triplet repeat-binding transcriptional regulator. It is regulated by SP1 and cell stress signals, and interacts with RNA polymerase II and the TFIID complex (TAFII32) to control transcription of CGG repeat-containing genes including FMR1 and rRNA genes. CGGBP1 also associates with DNA-PK, linking it to DNA damage response and chromatin organization. These molecular interactions place CGGBP1 at the nexus of transcriptional control, repeat biology, and genome stability.
Disruption of CGGBP1 in the Raji B-cell background provides a physiologically relevant model to examine its function in immune cell biology and lymphomagenesis. EBV-driven transcriptional programs in Raji cells may intersect with CGGBP1-mediated regulation of CGG repeat loci. Loss of CGGBP1 can reveal how alterations in repeat-dependent transcription impact B-cell proliferation, apoptosis, and antigen presentation. Moreover, studying this knockout in a transformed lymphoid setting allows assessment of CGGBP1’s role in chromatin organization and DNA damage signaling, processes often dysregulated in Burkitt lymphoma.
This polyclonal knockout cell population supports diverse assays: Western blotting and RT-qPCR for target validation, ChIP-qPCR for binding studies, and RNA-seq for transcriptome-wide analysis. Functional assays such as flow cytometry, apoptosis and cell cycle analyses, and drug sensitivity testing enable detailed phenotypic characterization. Key research applications encompass mechanistic dissection of fragile X syndrome-related transcriptional silencing, investigation of CGGBP1 in B-cell lymphoma pathogenesis, and screening of small-molecule modulators targeting CGG repeat biology. For ordering information and technical support, contact Ascent Research.
