The ACSS2 Knockout Jurkat Polyclonal Cells offer a CRISPR/Cas9-edited polyclonal population of Jurkat cells with targeted disruption of the ACSS2 gene, enabling loss-of-function analysis in a well-established T-lymphoblast model. Generated via CRISPR/Cas9-mediated gene disruption, these polyclonal knockout cells provide a heterogeneous pool suitable for bulk metabolic and epigenetic studies, eliminating the need for clonal isolation.
The Jurkat cell line is an immortalized T lymphoblast model derived from a patient with acute T-cell leukemia, widely used for studying T-cell signaling and leukemogenesis. Jurkat cells provide a relevant host for examining the metabolic and epigenetic roles of ACSS2 in a transformed lymphoid background, and their robust growth and well-characterized biology facilitate reproducible knockout-based experiments.
ACSS2 (acyl-CoA synthetase short-chain family member 2) catalyzes the ligation of acetate to coenzyme A (CoA) to form acetyl-CoA, an essential metabolite for de novo lipid synthesis and protein acetylation. Its expression is transcriptionally controlled by SREBF1, SREBF2, and HIF1A, with acetate availability serving as a key nutrient signal. Downstream, acetyl-CoA is consumed by acetyl-CoA carboxylase (ACC) and fatty acid synthase (FASN) to drive fatty acid biosynthesis, and it also acts as a donor for the histone acetyltransferases p300 and CBP, which acetylate histone H3 and modulate chromatin accessibility. Thus, ACSS2 functions at the intersection of metabolism and epigenetics, with its activity dependent on ATP and CoA as cofactors.
In the context of Jurkat T-leukemia cells, ACSS2-mediated acetate utilization may underpin the biosynthetic and epigenetic requirements essential for rapid proliferation. Disruption of ACSS2 in these polyclonal knockout cells allows for the investigation of acetyl-CoA-dependent processes including lipid synthesis and histone acetylation, potentially revealing metabolic vulnerabilities in acute T-cell leukemia and other ACSS2-associated cancers such as hepatocellular carcinoma, breast cancer, and glioblastoma.
This product is compatible with multiple assay modalities: Western blotting detects ACSS2 protein reduction; 13C-acetate tracing tracks metabolic flux; LC-MS quantifies acetyl-CoA levels; ChIP-qPCR assesses histone H3 acetylation; and proliferation or fatty acid synthase activity assays measure functional outcomes. For further details or technical inquiries, please reach out to Ascent Research.
