The DOCK11 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat T lymphocyte cell line. This product provides a loss-of-function model for DOCK11, a guanine nucleotide exchange factor (GEF) for Cdc42, enabling the study of its role in actin cytoskeletal regulation and immune cell signaling. The polyclonal format ensures a heterogeneous knockout population, suitable for pooled functional screening and bulk biochemical analyses without clonal selection pressures. The CRISPR-mediated gene disruption ablates DOCK11 expression, facilitating investigations into its downstream signaling consequences.
The host Jurkat cell line is an immortalized human T lymphocyte model originally derived from the peripheral blood of a patient with acute lymphoblastic leukemia. Jurkat cells are widely employed to study T cell receptor (TCR) signaling, apoptosis, and leukemia biology. Their robust growth characteristics and well-characterized signaling pathways make them an ideal platform for genetic manipulation, allowing researchers to dissect molecular mechanisms underlying T cell activation and immune disorders.
DOCK11 functions as a specific GEF for the small GTPase Cdc42, catalyzing the exchange of GDP for GTP to activate Cdc42. Upon activation, Cdc42 interacts with downstream effectors such as PAK kinases and the WASP/WAVE complex, promoting actin polymerization via the Arp2/3 complex. This signaling axis is triggered upstream by TCR engagement, chemokine receptors (e.g., CXCR4), and PI3K/Akt pathway activation. DOCK11 forms a complex with ELMO1, facilitating its GEF activity and linking extracellular cues to cytoskeletal remodeling. Consequently, DOCK11-mediated Cdc42 activation regulates cell morphology, migration, and immune cell effector functions.
In the context of Jurkat T cells, disruption of DOCK11 impairs Cdc42-dependent actin reorganization, thereby affecting cell adhesion, migration, and TCR-mediated activation. This knockout model recapitulates features of immune dysregulation observed in primary immunodeficiencies and autoimmune diseases, where DOCK11 mutations have been implicated. By eliminating DOCK11, researchers can dissect its contribution to T cell signaling independently of other Rho GTPase regulators, providing a clean background for structure-function studies and therapeutic target evaluation.
This polyclonal knockout cell population is suitable for a broad range of experimental applications, including flow cytometric analysis of T cell activation markers (CD69, CD25), western blotting for phosphorylated signaling intermediates (PAK, ERK), Transwell migration assays, and immunofluorescence staining of actin filaments with phalloidin. Additionally, it supports apoptosis assays (Annexin V staining) to assess cell survival defects. Researchers can utilize this model for drug target validation in autoimmune diseases, screening for immunological phenotypes, and investigating the interplay between DOCK11-regulated actin dynamics and T cell function. For further technical details, please contact Ascent Research.
