The CCPG1 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-cell leukemia line. This product provides a mixed pool of cells carrying targeted disruptions in the CCPG1 gene, enabling loss-of-function studies without clonal isolation. The polyclonal format preserves heterogeneity and is suitable for experiments where population-level effects of CCPG1 ablation are of interest. As a gene-edited model, these cells allow researchers to interrogate CCPG1-dependent processes in a T-lymphocyte background, offering a valuable tool for cancer cell biology and ubiquitin-proteasome system research.
The host Jurkat cell line is an immortalized human T-cell leukemia line of CD4+ T-lymphocyte origin, extensively used as a model for T-cell signaling, activation, and oncogenic transformation. These cells retain features of the adaptive immune response and are susceptible to genetic manipulation, making them a widely adopted platform for dissecting molecular pathways in a leukemic context. Their rapid proliferation and well-characterized signaling networks facilitate high-throughput screening and mechanistic studies. The Jurkat background is particularly relevant for investigating how alterations in cell cycle control and ubiquitin-mediated degradation contribute to T-cell malignancies.
CCPG1 encodes the substrate recognition component of an SCF (SKP1-CUL1-F-box protein) E3 ubiquitin ligase complex. The protein assembles with SKP1, CUL1, and RBX1 to form a functional ligase that targets specific proteins for ubiquitination and subsequent degradation by the 26S proteasome. CCPG1 is under the transcriptional control of the E2F1 transcription factor, linking its expression to cell cycle entry. Through its F-box domain, CCPG1 recruits substrates, including key cell cycle regulators such as cyclins and CDK inhibitors, for polyubiquitination. Disruption of CCPG1 thus impairs the timely proteolysis of these factors, potentially leading to uncoordinated cell cycle progression.
In the Jurkat T-cell leukemia context, knockout of CCPG1 disrupts an important node of the ubiquitin-proteasome pathway, likely affecting proliferation and survival. As a component of the SCF complex, CCPG1 participates in maintaining normal cell cycle transitions; its loss may promote uncontrolled division, a hallmark of cancer. This polyclonal knockout model therefore mimics a scenario of SCF ligase dysfunction relevant to leukemogenesis. By eliminating the substrate-recognition function, researchers can study how the resulting accumulation or depletion of downstream targets alters T-cell biology and contributes to oncogenic phenotypes.
These CCPG1 knockout Jurkat cells are suited for diverse experimental applications. Typical assays include Western blotting for cell cycle-related proteins (e.g., cyclin D1, p27), flow cytometric DNA content analysis to assess cell cycle distribution, and co-immunoprecipitation to examine SCF complex integrity. Researchers can employ RT-qPCR to measure E2F1 and CCPG1 transcript levels, MTT or CFSE proliferation assays to quantify growth, and apoptosis detection following drug treatment. The cells are especially valuable for screening sensitivity to proteasome inhibitors like bortezomib and for dissecting E2F1-driven oncogenic programs. For further information or technical support, please contact Ascent Research.
