The CDK7 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population that provides a loss-of-function model for studying the cyclin-dependent kinase 7 (CDK7) gene in a B-cell lymphoma context. This product consists of a heterogeneous pool of Raji cells engineered to disrupt CDK7 expression, enabling investigation of its dual roles in cell cycle regulation and transcription without the need for single-cell clonal isolation. The polyclonal format captures the variability inherent in CRISPR-mediated gene disruption, making it suitable for functional genomics, drug target validation, and pathway analysis.
Derived from the Raji human B lymphocyte cell line, an EBV-positive Burkitt’s lymphoma model, these cells are immortalized and widely employed in cancer biology and immunology research. Raji cells originate from a patient with Burkitt’s lymphoma and retain key oncogenic features, including constitutive MYC activation and continuous proliferation. Their well-characterized background facilitates studies of B-cell malignancies, therapeutic responses, and gene function in a lymphoma-relevant context.
CDK7 is the catalytic subunit of CDK-activating kinase (CAK), where it phosphorylates CDK1, CDK2, CDK4, and CDK6 to promote cell cycle progression, and it is a core component of the transcription factor II H (TFIIH) complex, phosphorylating RNA polymerase II C-terminal domain (CTD) at Ser5 and Ser7 to regulate transcription initiation and elongation. CDK7 kinase activity is positively regulated by Cyclin H and MAT1, which form the active CAK complex, and negatively modulated by CDK inhibitors such as p21 and p27, as well as CK2-mediated phosphorylation and DNA damage signals. It interacts with TFIIH subunits including XPB and XPD, RNA polymerase II, and the Mediator component MED1. Disruption of CDK7 eliminates these phosphorylation events, resulting in defective activation of downstream CDKs and impaired Pol II CTD phosphorylation, which together cause cell cycle arrest, global transcriptional downregulation??particularly of oncogenic drivers like MYC??and apoptosis.
In Raji B lymphocytes, which exhibit deregulated MYC expression and transcriptional addiction for sustained proliferation, CDK7 knockout dissects the interdependence of cell cycle and transcriptional control mechanisms. This model is especially relevant for evaluating CDK7-targeted therapies in B-cell malignancies, as it recapitulates the dual inhibition of CDK activation and Pol II phosphorylation that underlies the anti-tumor efficacy of pharmacological CDK7 inhibitors. It provides a physiologically relevant platform to study sensitivity, resistance, and the cellular consequences of CDK7 loss in a lymphoma background.
Researchers can apply this polyclonal knockout population to validate CDK7 inhibitors such as THZ1, perform drug sensitivity and resistance assays, and explore the interplay between cell cycle and transcription. Representative assays include Western blot for CDK7, phosphorylated CDKs, and phospho-Pol II; RT-qPCR for target gene expression changes; RNA-seq for global transcriptional profiling; and flow cytometry to analyze cell cycle distribution and apoptosis. Immunofluorescence can assess Pol II localization, and the model is suitable for CRISPR-based genetic screens. For further information contact Ascent Research.
