ADI1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ADI1 gene. This loss-of-function model utilizes the Jurkat T-lymphocyte background to enable studies of acireductone dioxygenase 1 in relevant disease contexts. The polyclonal format provides a population-level gene disruption, avoiding biases introduced by clonal selection.
Jurkat cells are an immortalized human T-lymphocyte line derived from the peripheral blood of a 14-year-old male with acute T-cell leukemia. Widely used as a model for T-cell acute lymphoblastic leukemia (T-ALL) and T-cell receptor signaling, these cells offer a robust platform for investigating oncogenic mechanisms and metabolic dependencies in lymphoid malignancies.
ADI1 encodes acireductone dioxygenase 1, a key enzyme in the methionine salvage cycle that catalyzes the penultimate step in methionine regeneration, thereby maintaining intracellular methionine and S-adenosylmethionine (SAM) levels. Acting as a tumor suppressor, ADI1 is transcriptionally regulated by c-Myc, androgen receptor, and SP1, and physically interacts with c-Myc, 14-3-3??, MTAP, and ENOPH1. ADI1 knockout disrupts methionine salvage, reducing SAM pools and attenuating mTORC1 signaling through decreased phosphorylation of S6K1 and 4E-BP1. This alteration dampens c-Myc transcriptional output, leading to reduced expression of target genes such as ODC1, CCND1, and MCL1, and impairing polyamine biosynthesis and apoptosis regulation.
In Jurkat T-ALL cells, ADI1 loss creates a context for examining the convergence of methionine metabolism, mTORC1 signaling, and c-Myc-driven oncogenesis. By disrupting the methionine salvage cycle, the knockout model mimics metabolic stress conditions that heighten leukemogenic potential through deregulated proliferation and apoptosis, providing a tool to probe tumor suppressor functions and metabolic vulnerabilities in leukemia.
This product supports diverse applications, including dissection of methionine metabolism in T-ALL, investigation of c-Myc-dependent oncogenic mechanisms, synthetic lethal screening under methionine deprivation, and evaluation of PRMT5 or MAT2A inhibitors. Compatible techniques include Western blotting for c-Myc, mTOR, phospho-S6K1, and MCL1; RT-qPCR for ADI1, ODC1, and CCND1; flow cytometry for apoptosis and cell cycle; LC-MS metabolomics; proliferation assays; drug sensitivity testing; and colony formation. For further information, contact Ascent Research.
