The ANXA2 Knockout Jurkat Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphoblast cell line. This polyclonal mixture, generated through CRISPR/Cas9-mediated gene disruption of the ANXA2 locus, provides a robust loss-of-function model for investigating ANXA2-dependent processes. The polyclonal format preserves population-level heterogeneity while enabling functional studies of ANXA2 ablation without clonal selection artifacts.
Jurkat cells are a widely used T lymphoblast line originally isolated from the peripheral blood of a 14-year-old male with acute T-cell leukemia. These cells serve as an established model system for examining T-cell receptor (TCR) signaling, immune response mechanisms, and cytokine production. The immortalized nature of Jurkat cells facilitates scalable experiments on lymphocyte activation, signal transduction, and proliferation, making them particularly suited for genetic perturbation studies aimed at dissecting molecular pathways in T-cell biology.
ANXA2 encodes a calcium-dependent phospholipid-binding protein that functions as a cell surface receptor for plasminogen and tissue plasminogen activator (tPA), enhancing plasmin generation and extracellular matrix degradation. ANXA2 also forms a complex with S100A10 to regulate actin cytoskeleton reorganization, cell adhesion, and membrane trafficking. Upstream regulators include SRC kinase, EGF, calcium, and IL-6, while downstream signaling converges on plasmin activation, matrix metalloproteinase (MMP) activity, and NF-??B transcriptional responses. The protein interacts with integrins, caveolin-1, and actin, placing ANXA2 at a nexus coordinating fibrinolysis, cell migration, and pro-inflammatory signaling. Representative pathway components encompass ANXA2, S100A10, tPA, plasminogen, plasmin, integrins, FAK, and SRC, highlighting its role in adhesion and proteolytic cascades.
Within the Jurkat T-cell context, ANXA2 knockout is anticipated to impair cellular adhesion, migration, and activation-related signaling pathways. T lymphocytes rely on dynamic cytoskeletal rearrangements and integrin-mediated interactions for immune synapse formation and effector functions; ANXA2??s participation in these processes suggests that its disruption may attenuate TCR-dependent responses. Additionally, ANXA2 modulates plasmin-dependent extracellular matrix remodeling, a process increasingly recognized in lymphocyte trafficking and tissue invasion. Thus, this polyclonal knockout model offers a physiologically relevant system to dissect ANXA2??s contributions to T-cell biology, including activation kinetics, cytokine output, and adhesive properties.
This ANXA2 knockout Jurkat polyclonal cell population is valuable for a range of research applications, including investigations into cancer metastasis, fibrinolysis, cell migration, immune cell activation, and drug target validation. Typical experimental readouts include Western blotting and RT-qPCR for expression analysis, immunofluorescence and flow cytometry for phenotypic characterization, migration and invasion assays for functional assessment, plasmin activity assays to evaluate proteolytic capacity, co-immunoprecipitation to study protein interactions, and phospho-signaling analysis to map downstream pathways. For further information or to discuss custom requirements, please contact Ascent Research.
