CKM Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte line, featuring targeted disruption of the CKM gene. This loss-of-function model provides a powerful tool for investigating creatine kinase-dependent energy metabolism in lymphoid cancer cells. The polyclonal format reflects a heterogeneous population of edited cells, enabling study of gene-editing effects without clonal selection pressure.
Raji cells, an EBV-positive Burkitt’s lymphoma line established from a Nigerian patient, serve as a well-characterized model for B cell malignancies. They express CD19 and CD20, reflecting their mature B cell phenotype, and are widely used in immunology and cancer research. The EBV positivity makes this line particularly relevant for studying viral-lymphoma interactions and metabolic vulnerabilities.
CKM encodes muscle-type creatine kinase, which catalyzes the reversible transfer of phosphate from phosphocreatine to ADP to regenerate ATP, critical for energy buffering. In this knockout, disruption of CKM impairs the phosphocreatine shuttle, affecting ATP homeostasis. CKM expression is regulated by MyoD, myogenin, MEF2, HIF-1??, and AMPK, and responds to calcium signaling. Its activity directly interacts with creatine, ADP, and ATP, and functionally couples with myofibrillar proteins and mitochondrial creatine kinase (CKMT2) to sustain cellular energetics. Loss of CKM disrupts the phosphocreatine energy buffer, leading to altered ATP:ADP ratios and compromising metabolic flexibility under energy stress.
In the Raji lymphoid context, where creatine kinase is not typically expressed at high levels, this knockout enables dissection of ectopic roles of the creatine kinase system in B cell lymphoma. It may uncover dependencies on arginine?Ccreatine metabolism or compensatory pathways, highlighting potential therapeutic targets. The EBV-driven proliferation may sensitize cells to energy stress induced by CKM loss, making this model valuable for studying metabolic reprogramming in aggressive lymphomas.
Applications include metabolic flux analysis using Seahorse assays, ATP/ADP ratio measurement, cell viability and apoptosis assays, and flow cytometric assessment of proliferation. This knockout is suited for drug sensitivity screens targeting energy metabolism and for validating creatine kinase as a therapeutic target in hematological malignancies. Additionally, it can be used to study the interplay between EBV latency, oncogenic signaling, and metabolic regulation. For additional details or to request a quote, please contact Ascent Research.
