The HEG1 Knockout Jurkat Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of Jurkat cells harboring targeted disruption of the HEG1 gene. This loss-of-function model enables systematic investigation of HEG1-mediated cellular processes without the confounding effects of compensatory clonal selection observed in single-cell-derived lines. The polyclonal format preserves the genetic heterogeneity of the edited pool, making it suitable for population-based functional genomic studies and high-throughput screening applications.
Jurkat cells are an immortalized human T lymphocyte line derived from acute T cell leukemia. This well-characterized model recapitulates key aspects of T cell receptor signaling, cytokine production, and activation-induced apoptosis. The Jurkat background provides a physiologically relevant context for studying lymphocyte adhesion, immune synapse formation, and intracellular signaling networks. Its robust growth characteristics and ease of genetic manipulation make it a preferred platform for interrogating signaling pathways relevant to T cell biology and leukemia pathogenesis.
HEG1 is a transmembrane protein that coordinates cell adhesion, junction assembly, and Hippo pathway modulation by recruiting the scaffold protein Kibra (WWC1) to cell?Ccell contacts. At junctions, HEG1 facilitates activation of the LATS1/2 kinases, which phosphorylate the transcriptional co-activators YAP and TAZ, promoting their cytoplasmic retention and inhibiting TEAD-mediated transcription. Loss of HEG1 disrupts this regulatory axis, resulting in nuclear accumulation of YAP/TAZ and increased expression of target genes such as CTGF and CYR61. Additionally, HEG1 modulates Rho GTPase signaling; its deletion perturbs RhoA activity, altering ROCK-mediated phosphorylation of MLC and downstream actin cytoskeletal dynamics. HEG1 interacts with angiomotin (AMOT) and tight junction proteins, including ZO-1, thereby integrating upstream adhesive and mechanotransductive cues.
In the Jurkat T-cell context, HEG1 knockout cells are a valuable tool for dissecting Hippo pathway roles in immune function. Despite extensive study in epithelia, Hippo signaling in lymphocytes is underexplored. HEG1-dependent YAP/TAZ regulation may influence T cell adhesion, activation, and migratory behavior. Thus, this model enables investigation of how junctional and mechanical cues are transduced in leukemic T cells, with potential implications for lymphocyte infiltration and metastasis.
Key research applications include screening for YAP/TAZ modulators, investigating RhoA?CHippo crosstalk during T cell adhesion and migration, and assessing cell junction dynamics. Compatible assays encompass Western blotting for YAP/TAZ and phospho-YAP, flow cytometry for CD69 and CD25, RhoA activity pulldowns, immunofluorescence for junctional proteins, RT-qPCR for CTGF and CYR61, and Annexin V apoptosis staining. This polyclonal knockout population is well-suited for population-based studies requiring reproducibility across genetically diverse backgrounds. For further information, contact Ascent Research.
