The ARHGEF17 Knockout Jurkat Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes with targeted disruption of the ARHGEF17 gene. This polyclonal knockout cell pool provides a robust loss-of-function model that avoids the limitations of clonal selection, enabling researchers to study ARHGEF17-dependent processes in a heterogeneous cell context that better reflects native population variability. The cells retain the fast growth and signaling characteristics of the Jurkat parental line while allowing reproducible assessment of gene function in assays that require averaging across the knockout population.
Jurkat cells are an immortalized human T lymphocyte line derived from a patient with acute T cell leukemia. These cells are p53-deficient, which facilitates their continuous proliferation and renders them a widely used model system for investigating T cell receptor (TCR) signaling, apoptosis, and leukemia biology. Their lymphoid origin and well-characterized signaling pathways make them particularly suitable for examining the roles of guanine nucleotide exchange factors (GEFs) in immune cell function and oncogenic transformation.
ARHGEF17 encodes a RhoA-specific guanine nucleotide exchange factor that catalyzes GDP/GTP exchange on RhoA, triggering RhoA activation. Upstream inputs include integrin signaling, GPCRs, growth factor receptors such as EGFR, and mechanical stress. Activated RhoA stimulates ROCK, leading to phosphorylation of MLC and LIMK, which phosphorylates cofilin, promoting actin stress fiber formation, focal adhesion assembly, and actomyosin contractility. ARHGEF17 interacts with G??12/13 and PDZ domain-containing proteins, linking it to spatial actin regulation at cell junctions. Through RhoA?CROCK signaling, ARHGEF17 influences SRF-mediated transcription, coordinating cytoskeletal remodeling with gene expression programs for cell migration, adhesion, and polarity.
In Jurkat T cells, ARHGEF17-mediated RhoA activation is particularly relevant for processes such as lymphocyte polarization, migration, and adhesion, which are essential for immune surveillance and are dysregulated in leukemia metastasis. Disruption of ARHGEF17 in these polyclonal knockout cells enables dissection of the RhoA signaling axis independent of alternative GEFs, providing a clean background to assess the contribution of this exchange factor to T cell invasiveness and cytoskeletal organization. Given the p53-null background, these cells also offer a unique window into how ARHGEF17-driven adhesion and contractility intersect with genomic instability and survival pathways in acute lymphoblastic leukemia.
These polyclonal ARHGEF17 knockout Jurkat cells are ideal for RhoA-GTP pull-down assays to gauge RhoA activity, Western blotting for ROCK and MLC phosphorylation, and immunofluorescence visualization of actin stress fibers. They also support functional studies such as Transwell migration and adhesion assays. Researchers in Rho GTPase signaling, cancer metastasis, or T cell biology can apply these cells for drug target screening or pathway dissection. For custom assay development or bulk orders, please contact Ascent Research.
