The DMTN Knockout Jurkat Polyclonal Cells product comprises a polyclonal population of Jurkat cells subjected to CRISPR/Cas9-mediated gene disruption targeting the DMTN locus. This loss-of-function model enables researchers to investigate the functional consequences of dematin ablation in a human T lymphocyte background. The polyclonal nature provides a heterogeneous knockout population, reflecting a range of editing outcomes without clonal selection, which is suitable for studying averaged cellular responses and population-level phenotypes in T cell biology.
The host Jurkat cell line is an immortalized human T cell leukemia line originally derived from the peripheral blood of a 14-year-old male with T cell acute lymphoblastic leukemia. The E6-1 clone is widely employed as a model system for T cell receptor (TCR) signal transduction, apoptosis mechanisms, and HIV research. Its robust growth characteristics and well-defined signaling pathways make it an ideal chassis for CRISPR-based functional genomics studies.
The DMTN gene encodes dematin, an actin-bundling protein that orchestrates cytoskeletal architecture and membrane stability. Dematin functions downstream of TCR engagement, protein kinase A (PKA), protein kinase C (PKC), calmodulin, and Ras signals, and it interacts directly with actin, Grb2, Ras, adducin, spectrin, and Band 3 (SLC4A1). Through its association with Grb2, dematin participates in Ras-MAPK pathway modulation, linking extracellular cues to actin reorganization. This positions DMTN at a convergence point between cytoskeletal remodeling and mitogenic signaling cascades such as the Ras-Raf-MEK-ERK axis.
In Jurkat T cells, disruption of DMTN expression is anticipated to impair actin bundling, resulting in altered cell morphology, reduced immune synapse formation, and attenuated TCR-proximal signaling. Loss of dematin may disrupt the localization or activation of signaling complexes containing Grb2 and Ras, thereby dampening downstream phosphorylation of ERK and other effectors. This knockout model therefore provides a valuable tool to dissect the interplay between actin dynamics and T cell activation, with implications for leukemia cell adhesion and motility.
This polyclonal knockout product is suited for a range of experimental applications, including flow cytometric analysis of activation markers, Western blotting for phospho-ERK, immunofluorescence visualization of the actin cytoskeleton, and adhesion or migration/invasion assays. It also supports T cell activation assays measuring IL-2 secretion and co-immunoprecipitation studies of Grb2-Ras complexes. Researchers investigating Ras-MAPK pathway inhibitors or the role of dematin in hereditary spherocytosis will find this model useful. For further information or technical support, please contact Ascent Research.
