The AIMP1 Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population with targeted disruption of the AIMP1 gene. This engineered Jurkat model provides a defined loss-of-function system to interrogate AIMP1??s dual role as a structural component of the multisynthetase complex and as a secreted cytokine. The polyclonal format offers a heterogeneous pool of edited cells, facilitating pooled functional studies without clonal bias. Researchers can investigate how AIMP1 deficiency impacts T cell biology, translation fidelity, and cytokine-mediated signaling.
The Jurkat cell line is an immortalized human T lymphocyte model derived from a patient with T cell acute lymphoblastic leukemia (T-ALL). Widely used in immunology and oncology research, these suspension cells serve as a robust system for studying T cell receptor signaling, apoptosis, and leukemogenesis. The Jurkat background provides a physiologically relevant environment for exploring AIMP1 functions in malignant T cells, retaining key signaling features that make it suitable for dissecting AIMP1??s contributions to immune cell activation and survival.
AIMP1 functions intracellularly as a scaffold within the multi-tRNA synthetase complex, interacting with KRS, MRS, AIMP2, and AIMP3 to facilitate efficient tRNA aminoacylation. Upon secretion triggered by IFN-??, TNF-??, or cellular stress, AIMP1 acts as a cytokine that binds integrin ??v??3 to activate downstream effectors including ERK, p38 MAPK, NF-??B, and caspases. This signaling cascade mediates apoptosis induction, inhibition of angiogenesis, and modulation of immune responses. Disrupting AIMP1 expression in this model enables dissection of both its translation machinery role and its receptor-mediated cytokine functions.
In the Jurkat T-ALL context, AIMP1 knockout disrupts the multisynthetase complex stoichiometry, potentially altering aminoacyl-tRNA synthesis and global protein translation??processes often dysregulated in leukemia. Simultaneously, abrogation of secreted AIMP1 eliminates its autocrine/paracrine effects on T cell survival, apoptotic induction, and angiogenic signaling. This dual perturbation helps delineate AIMP1??s contributions to leukemic cell behavior and its interaction with microenvironmental cues. The model also offers insights into conserved stress pathways relevant to AIMP1-linked neurodegeneration, such as hypomyelinating leukodystrophy.
The polyclonal AIMP1 knockout cells are designed for diverse experimental applications. Gene disruption can be confirmed by Sanger sequencing and RT-qPCR, while protein loss is assessed via Western blotting. Functional analyses include flow cytometry for apoptosis and surface markers, cytokine secretion ELISA, and co-immunoprecipitation to assess multisynthetase complex integrity with KRS and AIMP2. Translation efficiency can be evaluated by puromycin incorporation, and global transcriptome changes via RNA-seq. The model supports high-throughput screening for modulators of AIMP1-mediated apoptosis or angiogenesis and in-depth mechanistic studies integrating integrin ??v??3, NF-??B, and caspase activation. For additional technical details, contact Ascent Research.
