The AIMP2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the AIMP2 gene in the Jurkat human T lymphocyte line. As a polyclonal pool, this product provides a heterogeneous mixture of genotypes suitable for population-level functional analyses, enabling robust investigation of AIMP2-dependent signaling pathways without clonal bias.
Jurkat cells are an immortalized T lymphocyte line derived from an acute lymphoblastic leukemia patient. They grow in suspension, express CD3 and the T cell receptor, and are extensively used to model T cell signaling, activation, and apoptosis. This cell line is a cornerstone in immunology and cancer research, particularly for dissecting T cell receptor pathways, cytokine responses, and apoptotic mechanisms. Their well-characterized genetics, rapid proliferation, and amenability to genetic manipulation make them an ideal host for CRISPR/Cas9-mediated gene disruption studies.
AIMP2 is a multifunctional protein that, under basal conditions, scaffolds the multi-tRNA synthetase complex. Upon DNA damage, it dissociates and translocates to the nucleus to bind MDM2, inhibiting its ubiquitin ligase activity and stabilizing p53. Stabilized p53 transactivates downstream genes such as CDKN1A (p21), BAX, and PUMA, triggering cell cycle arrest and apoptosis. Upstream kinases ATM and ATR phosphorylate AIMP2, promoting its release from the synthetase complex. AIMP2 also interacts with TRAF2, linking it to JNK-mediated stress signaling and caspase cascades. Therefore, AIMP2 serves as a molecular switch coupling translational fidelity to genomic surveillance, and its disruption compromises p53-dependent tumor suppression.
In Jurkat cells, which retain wild-type p53, AIMP2 knockout impairs the DNA damage-induced apoptotic response, enhancing survival and mimicking oncogenic events relevant to T cell leukemia. This model allows dissection of AIMP2??s role in p53-mediated apoptosis, DNA damage response, and its contribution to chemoresistance. Comparative studies can reveal how loss of AIMP2 alters sensitivity to genotoxic chemotherapeutics, providing a platform for drug discovery and validation of p53-activating compounds in a leukemia-relevant background.
Representative applications include Western blotting and RT-qPCR for p53, MDM2, and downstream targets; Annexin V/PI flow cytometry to quantify apoptosis after UV or etoposide treatment; co-immunoprecipitation of AIMP2 with MDM2 or synthetase components; p53 luciferase reporter assays; and cell cycle analysis to evaluate checkpoint integrity. Dose-response viability curves following genotoxic challenge can delineate differential chemosensitivity attributable to AIMP2 status. The polyclonal knockout format is particularly suited for functional screening and pooled phenotypic assays where heterogeneous editing reflects diverse genetic perturbations. For detailed product inquiries, protocols, or custom gene-edited cell models, please contact Ascent Research.
