The CUTC Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji B lymphocytes, featuring targeted disruption of the CUTC gene. This product provides a genetically heterogeneous loss-of-function model suitable for investigating CUTC-dependent copper homeostasis in a lymphoblastoid background. The polyclonal format captures naturally occurring variation in knockout efficiency and clonal responses, enabling robust population-level studies.
Raji cells are a widely used human B lymphoblastoid line established from a Burkitt’s lymphoma patient. They retain key features of mature B cells, including antibody production and antigen presentation capabilities, making them a relevant model for B lymphocyte biology and hematological malignancies. The Raji line is particularly valuable for studying signaling pathways that govern B cell proliferation, survival, and immune function, as well as for evaluating oncogenic mechanisms in lymphoma.
CUTC encodes a copper transporter that mediates copper uptake and intracellular distribution, playing a central role in copper homeostasis. Its expression is regulated by metal-regulatory transcription factor 1 (MTF1) and intracellular copper levels, while it functionally interacts with copper chaperones ATOX1 and CCS. Downstream targets include SOD1 and COX17, both copper-dependent enzymes crucial for oxidative stress defense and mitochondrial respiration. By facilitating copper delivery to cuproenzymes, CUTC integrates into a broader network involving copper importers (CTR1), exporters (ATP7A, ATP7B), and sensors that coordinate cellular copper status. Disruption of CUTC is expected to impair copper distribution, leading to reduced activity of SOD1, COX17, and other cuproenzymes, thereby altering redox balance and potentially triggering cuproptosis.
In the context of Raji B cells, CUTC knockout provides a platform to dissect copper-dependent vulnerabilities in malignant B lymphocytes. Given the role of copper in cell proliferation and oxidative stress management, loss of CUTC may sensitize these lymphoma-derived cells to copper depletion or overload, uncovering metabolic dependencies relevant to hematological cancers. This model is particularly suited to explore cuproptosis??a recently described copper-induced cell death pathway??and its interplay with oncogenic signaling in Burkitt’s lymphoma.
Researchers can apply this knockout model to investigate copper metabolism in B lymphocytes, screen for copper-dependent therapeutic targets in lymphoma, and assess the impact of copper dysregulation on immune cell function. Representative experimental approaches include copper uptake and efflux assays, Western blotting for SOD1 and COX17, qRT-PCR for copper-responsive genes such as MT1A and MT2A, cell viability assays under copper challenge, flow cytometric measurement of oxidative stress and apoptosis, and proliferation analyses. These tools enable detailed mechanistic studies and drug screening efforts focused on metal ion homeostasis. For further information or custom inquiries, please contact Ascent Research.
