The ARHGAP18 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T lymphocyte line. This product features targeted disruption of the ARHGAP18 gene, generating a loss-of-function model for investigating Rho GTPase signaling and actin cytoskeletal regulation in a T cell context. The polyclonal format comprises a heterogeneous collection of edited cells, reflecting diverse CRISPR/Cas9-mediated gene disruptions across the population, making it suitable for experiments where bulk functional analysis captures collective pathway effects without clonal selection bias.
Jurkat cells are an immortalized T lymphocyte line established from a patient with acute T cell leukemia. They serve as a widely adopted model system for studying T cell receptor signaling, immune synapse formation, and leukemia biology due to their robust proliferation and genetic tractability. This cellular background provides a physiologically relevant platform to interrogate molecular mechanisms controlling T cell activation, adhesion, and migration, processes that are often dysregulated in hematological malignancies.
ARHGAP18 encodes a Rho GTPase-activating protein that functions as a negative regulator of the small GTPases RhoA and Cdc42. Its enzymatic activity accelerates GTP hydrolysis, converting these molecular switches to their inactive GDP-bound states, thereby limiting actin stress fiber assembly, focal adhesion turnover, and cell contractility. Upstream activation of ARHGAP18 is influenced by integrin ligation, mechanical force, and TGF-?? signaling. The downstream consequences of ARHGAP18-mediated RhoA and Cdc42 inactivation are propagated through effectors such as ROCK, PAK, LIMK, cofilin, and myosin light chain, which collectively orchestrate actin polymerization and actomyosin contraction.
In Jurkat T cells, disruption of ARHGAP18 leads to hyperactivation of RhoA and Cdc42, resulting in increased actin stress fiber formation, enhanced cell contractility, and altered migratory properties. This dysregulation can impair T cell functions including adhesion, immune synapse formation, and activation, providing a compelling model to dissect how Rho GTPase signaling modulates T lymphocyte physiology. The knockout cells are particularly valuable for examining the role of ARHGAP18 in actin-dependent processes that underpin T cell motility and adhesive interactions.
Typical research applications encompass screening for regulators of cell migration in leukemia, investigating actin cytoskeleton dynamics during immune synapse assembly, and elucidating ARHGAP18’s contribution to T cell activation and adhesion. Representative assays include Western blotting for RhoA and Cdc42 activity, F-actin staining with phalloidin followed by confocal microscopy, transwell migration assays, adhesion assays, T cell activation assays measuring CD69 expression or IL-2 secretion, co-immunoprecipitation of Rho GTPases, phospho-signaling analysis of phospho-MLC, and flow cytometry for integrin expression. For further details or to inquire about custom cell solutions, please contact Ascent Research.
