This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population in the Jurkat T lymphocyte line, engineered to disrupt the CBS gene. The resulting loss-of-function model enables investigation of cystathionine beta-synthase (CBS) functions in human T cells. CBS plays a critical role in sulfur amino acid metabolism, and its genetic disruption provides a robust tool for dissecting homocysteine handling, H2S production, and redox homeostasis.
Jurkat cells are an immortalized human T lymphocyte line originally derived from the peripheral blood of a 14-year-old boy with T cell acute lymphoblastic leukemia. This cell line is widely employed in T cell biology, cancer research, and immunological studies, including HIV infection susceptibility assays. The Jurkat background offers a well-characterized model for examining signal transduction pathways, apoptosis, and cellular metabolism, making it suitable for studying CBS functions in a leukemic T cell context.
CBS catalyzes the condensation of homocysteine and serine to form cystathionine, a pivotal step in the transsulfuration pathway that links the methionine cycle to cysteine and glutathione synthesis and drives H2S generation. The enzyme is allosterically activated by S-adenosylmethionine and regulated by hydrogen peroxide, nitric oxide, and insulin. Downstream, CBS produces cystathionine, which is processed by cystathionine gamma-lyase (CTH) to cysteine, feeding into glutathione and H2S pools. H2S further promotes protein persulfidation and modulates NF-??B signaling. CBS also interacts with serine hydroxymethyltransferase (SHMT) and protein kinase A, integrating one-carbon metabolism with sulfur metabolism.
In Jurkat T cells, CBS knockout is expected to impair transsulfuration, leading to elevated homocysteine, reduced cystathionine and cysteine, diminished glutathione levels, and compromised H2S generation. These metabolic shifts disrupt redox balance and may alter H2S-driven signaling events, including NF-??B activity, which is relevant to T cell activation, proliferation, and survival. Consequently, this model allows dissection of how sulfur metabolism influences leukemic T cell biology, oxidative stress responses, and homocysteine-induced pathologies such as cardiovascular and neurological complications.
Researchers can utilize these CBS knockout Jurkat cells to explore homocysteine metabolism, H2S signaling in lymphocytes, redox regulation of T cell activation, and the role of transsulfuration in leukemia. Representative assays include Western blotting and RT-qPCR for pathway components, CBS enzyme activity assays, homocysteine quantitation, H2S production measurement using lead acetate or fluorescent probes, glutathione quantification, reactive oxygen species detection, and cell viability or apoptosis assays by Annexin V/propidium iodide staining. For additional information, contact Ascent Research.
