The CCDC90B Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T-lymphocyte line, engineered for targeted disruption of the CCDC90B gene. This loss-of-function model is generated through Cas9-mediated gene knockout, yielding a heterogeneous pool of edited cells suitable for functional studies of mitochondrial dynamics and cell death pathways in a leukemic background. As a polyclonal product, it preserves population-level representation of diverse editing events, enabling robust assessment of CCDC90B-dependent phenotypes without clonal selection bias.
The Jurkat host cell line originates from an acute T-cell leukemia patient and serves as a widely used model for T-cell receptor (TCR) signaling, cytokine production, and adaptive immunity. These suspension cells exhibit characteristic T-lymphoblast morphology and maintain key signaling networks, including those governing IL-2 secretion and activation-induced apoptosis. Their well-characterized genetic and functional landscape makes Jurkat cells an advantageous platform for interrogating genes with pleiotropic roles in both immune function and mitochondrial homeostasis.
CCDC90B encodes a mitochondrial outer membrane protein essential for maintaining mitochondrial network integrity by promoting fusion through direct interactions with the dynamin-like GTPases MFN2 and OPA1. Upstream, CCDC90B expression is regulated by the transcriptional coactivator PGC-1?? and the nuclear respiratory factor NRF1, linking mitochondrial biogenesis to fusion capacity. Downstream consequences of CCDC90B loss include fragmented mitochondrial morphology, altered ATP production, cytochrome c release modulation, and perturbation of oxidative phosphorylation and apoptosis signaling. In the context of mitochondrial dynamics, CCDC90B functions cooperatively with MFN2 and OPA1 to counterbalance DRP1-mediated fission, thereby sustaining mitochondrial architecture and bioenergetic function.
In Jurkat T cells, mitochondrial dynamics critically influence metabolic reprogramming, apoptosis sensitivity, and T-cell activation thresholds. Disruption of CCDC90B in this leukemic background may exacerbate mitochondrial fragmentation, altering the balance of pro- and anti-apoptotic signals and potentially impairing energy production required for robust TCR signaling and cytokine synthesis. This model thus provides a relevant tool for dissecting how mitochondrial fusion defects contribute to leukemia cell survival, drug resistance, and immune escape mechanisms.
Primary applications include high-content imaging of mitochondrial morphology via immunofluorescence, quantitative western blotting of MFN2 and OPA1 to assess fusion protein levels, and flow cytometric apoptosis assays using Annexin V staining to evaluate altered cell death sensitivity. Complementary functional analyses such as Seahorse extracellular flux analysis offer direct measurements of oxygen consumption rate and glycolytic activity, while RT-qPCR can profile expression changes in nuclear-encoded mitochondrial genes. The CCDC90B Knockout Jurkat Polyclonal Cells are ideal for drug sensitivity screening in leukemia and for investigative studies of mitochondrial contributions to neurodegenerative disease mechanisms. For ordering and technical inquiries, please contact Ascent Research.
