The LDHB Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte cell line. This product provides a heterogeneous pool of cells with targeted disruption of the LDHB gene, offering a robust loss-of-function model for studying lactate dehydrogenase B function. The polyclonal format preserves the diversity of editing outcomes, which can be advantageous for assessing overall gene disruption effects in a population context while maintaining the inherent characteristics of the parental line.
The Raji cell line is a well-characterized human Burkitt lymphoma cell line that is Epstein-Barr virus (EBV) positive and exhibits a lymphoblastoid morphology. Derived from a B lymphocyte lineage, these cells grow in suspension and are widely used as a model system for B-cell malignancies, particularly EBV-associated lymphomas. Raji cells retain key features of B cells and are instrumental in studying humoral immunity, lymphomagenesis, and tumor cell metabolism, making them an ideal host for interrogating metabolic gene function.
LDHB encodes the B subunit of lactate dehydrogenase, which catalyzes the interconversion of lactate and pyruvate coupled to the reduction of NAD+ to NADH. This enzymatic reaction is central to glycolysis and the Cori cycle, and is regulated by factors such as HIF-1 alpha, c-MYC, and p53, while modulating downstream mediators including the NAD+/NADH redox balance, ATP production, and reactive oxygen species (ROS) levels. LDHB functions in concert with LDHA to form tissue-specific LDH isoenzymes and interacts with other glycolytic enzymes like PKM2. The LDHB-mediated metabolic node is integral to energy homeostasis and cellular responses to hypoxia and metabolic stress.
In Raji Burkitt lymphoma cells, which exhibit a high glycolytic rate characteristic of the Warburg effect, disruption of LDHB expression is expected to perturb the balance between aerobic glycolysis and mitochondrial oxidative phosphorylation. This metabolic rewiring can influence cell proliferation, survival under hypoxic conditions, and apoptotic signaling. The polyclonal knockout population allows researchers to interrogate the net effect of LDHB loss on B-cell lymphoma metabolism without clonal artifacts, making it a valuable tool for dissecting metabolic vulnerabilities in aggressive B-cell malignancies.
Key applications include investigating the role of LDHB in the Warburg effect and metabolic reprogramming of Burkitt lymphoma, assessing LDH isoenzyme composition and its impact on NAD+/NADH homeostasis, and evaluating sensitivity to glycolysis-targeting therapeutics. Typical experimental readouts involve Western blot and RT-qPCR for expression validation, colorimetric lactate dehydrogenase activity assays, Seahorse metabolic flux analysis, flow cytometry for proliferation and apoptosis markers, and LC-MS-based metabolomics. Additionally, this model can be employed in co-culture systems to explore how LDHB knockout affects tumor?Cimmune cell interactions within the microenvironment. For more information, please contact Ascent Research.
