The MLYCD Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji human B lymphocytes, in which the MLYCD gene is disrupted to create a loss-of-function model for studying malonyl-CoA decarboxylase. This polyclonal product contains a heterogeneous mixture of gene-edited cells, enabling population-level analysis of metabolic and signaling pathways without clonal artifacts.
The Raji cell line is an immortalized B lymphocyte established from an EBV-positive Burkitt’s lymphoma patient. With a lymphoblastoid phenotype and germinal center-like features, Raji cells are widely used to investigate B-cell biology, lymphomagenesis, and immune responses. Their robust proliferation and well-defined signaling make them a valuable host for studying metabolic interactions in B-cell malignancies.
MLYCD encodes malonyl-CoA decarboxylase, which catalyzes the conversion of malonyl-CoA to acetyl-CoA, removing inhibition of CPT1 and enabling mitochondrial fatty acid oxidation. The enzyme sits at the intersection of fatty acid metabolism, AMPK signaling, insulin signaling, and PPAR pathways. Its activity is regulated by upstream factors such as AMPK, PPAR??, insulin, glucagon, and cAMP, while downstream targets include CPT1, acetyl-CoA, and lipid synthesis pathways. MLYCD interacts functionally with ACC (ACACA/ACACB), which generates malonyl-CoA, forming a substrate cycle. Knockout of MLYCD disrupts decarboxylation, leading to malonyl-CoA accumulation, CPT1 inhibition, and blockade of fatty acid oxidation, forcing metabolic adaptation.
In Raji B cells, MLYCD loss models metabolic reprogramming observed in lymphoma, where altered fatty acid oxidation supports proliferation. Accumulated malonyl-CoA likely impairs mitochondrial respiration, mimicking aspects of MLYCD deficiency and metabolic syndrome. This model enables dissection of AMPK/PPAR??- and insulin-mediated control of B-cell metabolism, linking lipid homeostasis to lymphoma biology and stress responses.
Research applications include studying fatty acid metabolism in B-cell lymphoma, metabolic drug target validation, and cancer metabolic reprogramming. Compatible assays include Western blotting and RT-qPCR for gene expression, LC-MS for malonyl-CoA and acetyl-CoA quantification, Seahorse flux analysis for mitochondrial function, lipid droplet staining, and cell viability/proliferation assays by flow cytometry. These tools support mechanistic and phenotypic dissection of MLYCD-dependent pathways. For further information, please contact Ascent Research.
