The LCLAT1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human Raji B lymphocyte line. This product features targeted disruption of the LCLAT1 gene, generating a heterogeneous loss-of-function model that avoids clonal selection biases. The polyclonal format preserves genetic variability, closely mimicking native cellular heterogeneity and enabling robust studies of LCLAT1-dependent mitochondrial processes.
The Raji cell line originates from an EBV-positive Burkitt??s lymphoma, serving as a well-established model for B cell biology, EBV latency, and lymphomagenesis. These suspension-adapted B lymphocytes maintain key signaling pathways and exhibit active mitochondrial metabolism, making them a relevant host for investigating mitochondrial dysfunction in a malignant B cell context.
LCLAT1 encodes a lysocardiolipin acyltransferase localized to the inner mitochondrial membrane, where it reacylates lysocardiolipin to cardiolipin??a phospholipid critical for cristae architecture, respiratory chain integrity, and cytochrome c retention. Under oxidative stress or elevated ROS, LCLAT1 upregulation drives aberrant cardiolipin remodeling. This pathogenic activity disrupts mitochondrial function, leading to cytochrome c release and caspase-mediated apoptosis. LCLAT1 operates in a network involving TAZ, cardiolipin synthase, and phospholipase A2, which collectively regulate cardiolipin homeostasis. The enzyme??s substrates include lysocardiolipin and acyl-CoA donors, while its dysregulation feeds into mitochondrial phospholipid imbalance and apoptotic signaling.
In Raji lymphoma cells, LCLAT1 knockout allows interrogation of cardiolipin-dependent mitochondrial integrity within an oncogenic background. Burkitt??s lymphoma cells often exhibit altered apoptotic thresholds and elevated mitochondrial respiration, rendering them sensitive to changes in phospholipid composition. Disrupting LCLAT1 in this model helps clarify how cardiolipin remodeling impacts bioenergetics, ROS generation, and survival signaling, offering insights into lymphoma metabolism and potential therapeutic vulnerabilities.
This polyclonal knockout product is suitable for applications including Western blotting and RT-qPCR for gene disruption verification, lipidomics for cardiolipin profiling, JC-1 and DCFDA assays for mitochondrial membrane potential and ROS detection, Annexin V flow cytometry for apoptosis, and Seahorse analysis for metabolic flux. Researchers can utilize it to study mitochondrial dysfunction in B cell lymphoma, screen compounds for metabolic disorders (e.g., obesity, non-alcoholic fatty liver disease, cardiomyopathy, Parkinson??s disease), and explore cancer metabolism. For further information or technical inquiries, contact Ascent Research.
