The CCDC117 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-lymphoblast cell line through targeted disruption of the CCDC117 gene. This loss-of-function model provides a powerful tool for investigating the role of the coiled-coil domain-containing protein CCDC117 in T-cell acute lymphoblastic leukemia (T-ALL) biology. The polyclonal format preserves population-level heterogeneity, enabling robust statistical analysis of gene function in signaling networks and cellular phenotypes without clonal selection artifacts.
Jurkat cells, originally isolated from the peripheral blood of a 14-year-old male with acute lymphoblastic leukemia, serve as an extensively characterized model for T-cell signaling, apoptosis, and HIV infection. The Jurkat clone E6-1 exhibits constitutive activation of T-cell receptor signaling pathways and is widely employed to study oncogenic mechanisms in T-ALL. Their rapid proliferation, suspension growth characteristics, and well-defined genetic background make them ideal for high-throughput screening and mechanistic studies.
CCDC117 encodes a coiled-coil domain protein implicated in the regulation of cell proliferation, migration, and invasion, potentially through modulation of the PI3K/AKT signaling axis. This protein interacts with HSP90 and AKT, and functions downstream of growth factor receptors such as EGFR and IGF1R, as well as oncogenic drivers like RAS and MYC. Through these interactions, CCDC117 influences the expression of downstream targets including CCND1, MYC, BCL2, and MMP9, thereby orchestrating cell cycle progression, survival, and extracellular matrix remodeling. Representative pathway components connecting CCDC117 to these outputs include PI3K, AKT, mTOR, GSK3??, ??-catenin, and TCF/LEF transcription factors.
Knockout of CCDC117 in Jurkat cells enables direct dissection of its contribution to T-ALL pathophysiology, particularly in the context of AKT-dependent signaling and crosstalk with the Wnt/??-catenin pathway. Given the central role of AKT in promoting leukemic cell survival and proliferation, this model allows researchers to assess how loss of CCDC117 alters phospho-AKT levels, ??-catenin stabilization, and TCF/LEF-mediated transcription. The cellular background retains critical features of T-ALL, making the knockout population a relevant system for evaluating oncogenic dependency on CCDC117.
This product is suited for a wide range of experimental applications, including Western blotting to quantify AKT, phospho-AKT, and ??-catenin protein levels; RT-qPCR to measure CCND1 and MYC transcript abundance; flow cytometry for cell cycle distribution and apoptosis assays; and Transwell migration or Matrigel invasion studies. The polyclonal cells can also be used in xenograft mouse models to evaluate tumorigenic potential and therapeutic response in vivo, supporting preclinical cancer drug discovery efforts. For detailed product specifications, validation data, or technical support, please contact Ascent Research.
