The DECR1 Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-mediated polyclonal knockout population targeting the human DECR1 gene in the Raji B lymphoblastoid cell line. This product offers a heterogeneous pool of gene-disrupted cells, circumventing clonal isolation and enabling functional screening in a biologically relevant background for immediate use in metabolic and cancer research applications.
Raji is a continuous human B lymphoblastoid line originating from a Burkitt lymphoma patient. It carries Epstein?CBarr virus (EBV) and retains germinal center B-cell features, including reliance on both glycolytic and fatty acid oxidation pathways for energy and biosynthesis. The Raji model is extensively utilized to investigate B-cell malignancies, immune cell signaling, and metabolic adaptations driving lymphoma progression.
DECR1 encodes the mitochondrial 2,4-dienoyl-CoA reductase, an enzyme essential for the complete ??-oxidation of polyunsaturated fatty acids. It catalyzes the NADPH-dependent reduction of 2,4-dienoyl-CoA intermediates to 3-enoyl-CoA, overcoming the blockage posed by double bonds at even-numbered positions. DECR1 functions within a multi-enzyme ??-oxidation complex that includes enoyl-CoA hydratase, 3-ketoacyl-CoA thiolase, and electron transfer flavoproteins (ETF). Its expression is activated by PPAR-?? and PPAR-?? transcription factors, co-regulated by PGC-1??, and induced by fatty acid ligands such as linoleic and arachidonic acid. Downstream, the reaction generates acetyl-CoA, NADH, and FADH2??key substrates for the TCA cycle and oxidative phosphorylation??thereby integrating unsaturated fat catabolism with mitochondrial energy production and citrate synthesis.
Disruption of DECR1 in Raji B cells impairs the capacity to oxidize polyunsaturated fatty acids, forcing a metabolic shift that may increase dependence on saturated fatty acids or glycolysis. This alteration can perturb lipid homeostasis, membrane phospholipid composition, and lipid-derived signaling molecules, potentially affecting pathways critical for lymphoma cell survival and proliferation. Given the high fatty acid oxidation rates observed in Burkitt lymphoma, the knockout model creates a metabolic vulnerability that can be exploited to study drug resistance mechanisms and identify synthetic lethal interactions.
This polyclonal knockout product is suitable for a range of functional assays, including fatty acid oxidation flux measurements using 14C-labeled palmitate, Seahorse mitochondrial respirometry, and LC?CMS-based metabolomics to profile acyl-carnitine species and TCA cycle intermediates. Additional applications encompass apoptosis detection by Annexin V staining, assessment of mitochondrial membrane potential with JC-1, and transcriptional analysis via RNA sequencing under lipid-depleted conditions. By enabling the dissection of unsaturated fatty acid metabolism in a lymphoblastoid context, these cells support research into metabolic reprogramming in B-cell lymphomas and the preclinical evaluation of metabolism-targeting therapies. For further details or to discuss custom configurations, please contact Ascent Research.
