LPGAT1 Knockout Raji Polyclonal Cells consist of a viable, CRISPR/Cas9-edited polyclonal population of Raji B lymphoblastoid cells carrying targeted disruption of the LPGAT1 gene. This population provides a heterogeneous loss-of-function model that retains the genetic complexity inherent to polyclonal editing, enabling robust functional studies without clonal selection bias. The use of CRISPR/Cas9-mediated gene disruption in this format supports flexible experimental designs for investigating mitochondrial lipid biology in a lymphoma-relevant context.
The Raji cell line is a suspension-adapted, Epstein-Barr virus (EBV)-positive human B lymphoblastoid line originally derived from a Burkitt lymphoma. Raji cells constitutively express characteristic B cell surface markers such as CD19 and CD20, and they serve as a well-established model for B cell lymphoma biology, antibody-dependent cellular cytotoxicity, and lymphocyte signal transduction. Their hematopoietic origin and EBV transformation status make them particularly relevant for examining metabolic reprogramming in B cell lymphomagenesis and immune cell function.
LPGAT1 encodes a lysophosphatidylglycerol acyltransferase that catalyzes the reacylation of lysophosphatidylglycerol to form phosphatidylglycerol, an essential precursor for cardiolipin synthesis. This activity is regulated upstream by transcription factors including SREBP1 and PPAR??, and is responsive to mitochondrial stress signals. LPGAT1 functions within a biosynthetic pathway that includes CDS1, PGS1, PTPMT1, and cardiolipin synthase CRLS1, directly interacting with PGS1 and TAM41 to coordinate mitochondrial phospholipid remodeling. The product phosphatidylglycerol is further converted to cardiolipin, a critical inner mitochondrial membrane phospholipid that maintains cristae architecture, supports oxidative phosphorylation complexes, and modulates intrinsic apoptosis.
Ablating LPGAT1 function in Raji B lymphoblastoid cells creates a powerful platform for dissecting the role of mitochondrial phospholipid metabolism in B cell lymphoma. Because Raji cells exhibit high glycolytic and oxidative metabolic demand, disruption of phosphatidylglycerol production can compromise mitochondrial membrane integrity and oxidative phosphorylation, potentially altering proliferation, survival, and drug sensitivity. This model thus directly links the LPGAT1-regulated lipid network to oncogenic signaling and immune cell homeostasis, and provides a human cell-based system complementary to neural models for studying LPGAT1-related neurodevelopmental disorders that are underpinned by mitochondrial dysfunction.
This product is ideally suited for a range of applications including quantitative lipidomic profiling by LC-MS, metabolic flux analysis using Seahorse analyzers, assessment of mitochondrial membrane potential via JC-1 staining, and functional apoptosis assays. Researchers can employ these polyclonal knockout cells to interrogate cardiolipin-dependent signaling, validate small-molecule modulators of phospholipid metabolism, and study the interplay between mitochondrial health and B cell receptor signaling. Flow cytometry and RT-qPCR provide orthogonal methods to confirm target disruption and downstream expression changes. For further technical details and ordering information, please contact Ascent Research.
