The ANKRD2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human Jurkat T cells with targeted disruption of the ANKRD2 gene. This knockout model is generated by CRISPR/Cas9-mediated gene editing, resulting in a heterogeneous pool of ANKRD2-deficient cells ideal for studying gene function in T-cell biology and Hippo signaling. As a polyclonal knockout, it avoids clonal artefacts and enables physiologically relevant functional genomics studies.
Jurkat is an immortalized T-lymphocyte line derived from a 14-year-old male with acute lymphoblastic leukemia, widely used for T-cell receptor (TCR) signaling, activation, apoptosis, and HIV infection research. These cells exhibit key features of T-cell biology, including TCR-mediated signal transduction and cytokine responses, providing a robust platform for investigating gene function in immunological contexts.
ANKRD2 (Ankyrin Repeat Domain 2) is a transcriptional co-regulator that primarily functions within the Hippo/YAP signaling axis. Mechanistically, ANKRD2 interacts with the transcriptional co-activators YAP and TAZ and facilitates their binding to TEAD transcription factors, thereby modulating the expression of target genes such as cyclin D1 and myogenin. ANKRD2 activity is regulated by mechanical and oxidative stress via the upstream kinases LATS1/2, which phosphorylate YAP/TAZ and promote their cytoplasmic retention through 14-3-3 binding. In addition to its well-established role in muscle development, ANKRD2 forms complexes with p53, NF-??B, and PML, linking it to apoptosis and stress responses. Consequently, disruption of ANKRD2 in Jurkat cells is expected to perturb YAP/TEAD-dependent transcription and alter the balance between proliferation and apoptosis.
In Jurkat T cells, the Hippo pathway is emerging as a significant regulator of immune cell function, though it remains underexplored compared to epithelial systems. ANKRD2 knockout in this leukemic T-cell background offers a unique tool to dissect YAP/TAZ-mediated transcriptional programs in T-cell activation, survival, and oncogenic transformation. Given ANKRD2’s association with dilated cardiomyopathy and skeletal myopathies, this model also facilitates cross-tissue studies of conserved stress-response mechanisms. The polyclonal nature of the knockout ensures that phenotypic readouts reflect population-level responses, which is particularly advantageous for investigating heterogeneous processes such as apoptosis and proliferation.
These ANKRD2 knockout Jurkat polyclonal cells enable a wide range of assays, including Western blotting and co-immunoprecipitation to assess ANKRD2 interaction with YAP, TAZ, and TEAD; RT-qPCR and RNA-seq to profile Hippo target genes such as CTGF and CYR61; TEAD luciferase reporter assays to measure transcriptional activity; and flow cytometry to quantify proliferation (Ki-67) and apoptosis (Annexin V). Additionally, they are suitable for Hippo pathway drug screening and functional complementation experiments. For further information on product specifications and technical support, please contact Ascent Research.
