The CBS Knockout Raji Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function investigation of the cystathionine beta-synthase (CBS) gene within a human B lymphocyte background. This gene-edited model consists of a bulk population of Raji cells harboring targeted disruption of the CBS locus, avoiding clonal selection biases and preserving population heterogeneity. The use of polyclonal knockout cells facilitates the study of CBS-dependent phenotypes in a context that more closely mimics the genetic diversity encountered in unselected cellular contexts.
Raji cells are an immortalized B lymphocyte cell line derived from an Epstein?CBarr virus (EBV)-positive Burkitt lymphoma. These cells exhibit EBV latency type III, characterized by expression of the full complement of latent viral genes, including EBNA-1, EBNA-2, EBNA-3, LMP-1, and LMP-2, and they retain high surface immunoglobulin M (IgM) expression. The latent EBV genome endows Raji cells with properties relevant for studying oncogenic signaling, immune cell biology, and viral latency, making them a widely used model in immunology and cancer research.
Cystathionine beta-synthase (CBS) catalyzes the condensation of serine and homocysteine to form cystathionine, committing homocysteine to the transsulfuration pathway. CBS is allosterically activated by S-adenosylmethionine (SAM) and is subject to regulation by nitric oxide (NO) and heme, while its transcription is governed by SP1 and NF-Y. Downstream of CBS, cystathionine is cleaved by cystathionine gamma-lyase (CTH) to produce cysteine, ??-ketobutyrate, and hydrogen sulfide (H2S). CBS interacts with CTH, heme, SAM, and endothelial nitric oxide synthase (eNOS). Consequently, CBS disruption leads to homocysteine accumulation, impaired cysteine biosynthesis, reduced H2S production, and altered glutathione synthesis, thereby perturbing cellular redox balance.
In the Raji B lymphocyte context, knockout of CBS provides a powerful tool to dissect the role of the transsulfuration pathway in B cell physiology and lymphomagenesis. Given that B cells undergo dynamic changes in redox status during activation, differentiation, and malignant transformation, the loss of CBS function allows researchers to examine how homocysteine metabolism and H2S signaling influence proliferation, apoptosis, and stress responses. Additionally, this model enables the exploration of metabolic interactions between EBV latency programs and host sulfur metabolism.
This polyclonal knockout cell population is suitable for a range of investigative applications, including analysis of homocysteine and cystathionine levels via LC-MS, confirmation of gene disruption by Western blot or RT-qPCR, H2S production assays, and flow cytometry-based apoptosis or viability assessments. The model can be employed in drug sensitivity screens to identify compounds that target metabolic vulnerabilities arising from CBS deficiency, and it serves as a platform for studying the intersection of redox signaling, one-carbon metabolism, and B cell malignancies. For further details or order inquiries, please contact Ascent Research.
