The JMJD7 Knockout Jurkat Polyclonal Cells are a heterogeneous cell population generated by CRISPR/Cas9-mediated disruption of the JMJD7 gene in the Jurkat host background. This polyclonal knockout product provides a pooled loss-of-function model, enabling researchers to study the functional consequences of JMJD7 ablation without clonal selection. The genomic modification disrupts JMJD7 expression, creating a versatile tool for investigating the role of this protein hydroxylase in translation termination, hypoxic signaling, and T cell biology. The polyclonal nature preserves population-level heterogeneity, which can be advantageous for capturing diverse cellular responses and reducing clone-specific artifacts in pooled screening or functional assays.
Jurkat cells are an immortalized human T lymphocyte line derived from an acute T cell leukemia patient. Widely employed in immunology and cancer research, they retain many characteristics of peripheral blood T lymphocytes, including the ability to undergo activation-induced signaling, cytokine secretion, and apoptosis. The Jurkat model is particularly suited for dissecting T cell receptor signaling, survival pathways, and mechanisms of leukemogenesis. Their rapid proliferation and well-characterized signaling networks make them a robust host for CRISPR-based gene editing, allowing efficient interrogation of gene function in a human T cell context.
JMJD7 encodes a Fe(II)/2-oxoglutarate-dependent oxygenase that specifically hydroxylates the translation termination factor eRF1 at its N-terminal domain. This post-translational modification enhances eRF1 interaction with the ribosomal 40S and 60S subunits, thereby promoting efficient stop codon recognition and translation termination fidelity. JMJD7 activity is regulated by upstream factors including hypoxia, the transcription factor HIF1A, and SP1, linking translational control to cellular oxygen levels. Downstream, hydroxylated eRF1 modulates translation termination efficiency, affecting mRNA surveillance and protein synthesis. The JMJD7?CeRF1?Cribosome axis constitutes a critical node connecting environmental stress to translational output.
In Jurkat T cells, JMJD7-mediated eRF1 hydroxylation likely influences translation termination decisions during hypoxia, a condition prevalent in the tumor microenvironment. Aberrant translation termination can drive readthrough or premature termination, altering the proteome and contributing to leukemic cell adaptation. Disrupting JMJD7 in this T cell leukemia model permits dissection of how hypoxia-induced translational reprogramming affects cell growth, survival, and stress responses. The knockout cells may also reveal synthetic vulnerabilities or altered signaling dynamics that are otherwise masked in wild-type Jurkat cells.
This knockout tool is suited for a range of applications, including Western blot analysis of JMJD7 and hydroxylated eRF1 levels, co-immunoprecipitation to validate JMJD7?CeRF1 interaction, polysome profiling to interrogate translation termination efficiency, and luciferase-based stop codon readthrough reporters. The cells can be used in viability assays under normoxic versus hypoxic conditions to assess dependence on JMJD7 activity, as well as flow cytometry for apoptosis markers. Researchers may also perform RT-qPCR to monitor hypoxia-responsive gene expression changes. For ordering or technical inquiries, please contact Ascent Research.
