ARHGAP17 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of the ARHGAP17 gene in T-lymphocyte biology. This product consists of a heterogeneous pool of Jurkat cells carrying CRISPR/Cas9-mediated gene disruption of ARHGAP17, enabling loss-of-function analysis without the bias of clonal selection. The polyclonal format provides a more representative model of population-level gene inactivation, suitable for investigating ARHGAP17??s role in actin dynamics, cell polarity, and signaling.
The Jurkat cell line, derived from a 14-year-old male with acute T-cell leukemia (established 1976), is a suspension-adapted T-lymphocyte model expressing CD3, CD4, and functional TCR/CD3 complexes. It is widely used to study TCR signaling, T-cell activation, and apoptosis, and provides a well-characterized system for dissecting molecular mechanisms in immune cell function and leukemic transformation.
ARHGAP17 (Rich1) is a Rho GTPase-activating protein that specifically promotes GTP hydrolysis on Cdc42 and RhoA, thereby inactivating these small GTPases. This regulation leads to downstream suppression of PAK and ROCK kinases, reorganization of F-actin, and stabilization of tight junction proteins including occludin and ZO-1. ARHGAP17 acts downstream of Ephrin-A1/EphA2 and Netrin-1/DCC receptor signaling and is modulated by direct interactions with angiomotin, the STRIPAK complex, and cerebral cavernous malformation proteins CCM2 and CCM3. Through these pathways, ARHGAP17 coordinates actin cytoskeletal remodeling, cell polarity, and junctional integrity.
In Jurkat T cells, ARHGAP17-mediated control of Cdc42 and RhoA activity is critical for processes such as immune synapse formation, polarized migration, and adhesion. Knockout of ARHGAP17 in this polyclonal population permits investigation of how disrupted Rho GTPase signaling affects T-cell transendothelial migration, tight junction-like structures, and leukemic cell behavior, linking these to broader mechanisms of vascular permeability and inflammation.
Typical research applications include Western blotting for active Cdc42/RhoA, immunofluorescence for F-actin and tight junction markers, migration and invasion assays, and co-immunoprecipitation of angiomotin complexes. These tools enable dissection of ARHGAP17 function in TCR signaling, cell polarity, and junction regulation. For further details or support, please contact Ascent Research.
