The DOCK2 Knockout HAP1 Polyclonal Cells comprise a polyclonal population of the HAP1 cell line engineered with CRISPR/Cas9-mediated disruption of the DOCK2 gene. This polyclonal knockout cell model provides a functional loss-of-function system for investigating DOCK2-dependent processes without the limitations of single-clone selection, offering a population-level representation of gene disruption.
HAP1 is a near-haploid human cell line derived from a male patient with chronic myeloid leukemia (CML). Exhibiting an adherent fibroblast-like morphology and a near-haploid karyotype, this line is particularly advantageous for genetic manipulation and functional genomics studies. Its hematopoietic/myeloid origin makes it suitable for modeling signaling pathways pertinent to immune cell function, while the reduced gene copy number simplifies CRISPR/Cas9 editing and minimizes confounding genetic complexity.
DOCK2 encodes a Rac guanine nucleotide exchange factor (GEF) critical for actin cytoskeleton remodeling. It is activated downstream of chemokine receptors (e.g., CXCR4, CCR7), T cell receptors (TCR), and B cell receptors (BCR), forming a complex with ELMO1 or ELMO2 to catalyze GDP/GTP exchange on Rac1 and Rac2. This leads to activation of PAK kinases, the WAVE complex, and the Arp2/3 complex, orchestrating actin polymerization, cell polarization, and directed migration. DOCK2 thus functions as a central mediator of chemokine signaling, lymphocyte migration, and immune synapse formation.
In the near-haploid myeloid background of HAP1 cells, disrupting DOCK2 provides a unique model to dissect Rac-dependent actin dynamics and chemotactic responses in a simplified genetic environment. This knockout system is valuable for exploring the molecular underpinnings of immune cell trafficking, with direct relevance to immunodeficiencies, inflammatory disorders, and autoimmune diseases. Additionally, DOCK2-related signaling aberrations have been implicated in certain cancers, expanding the model’s utility to cancer biology research.
Researchers can employ this DOCK2 knockout model in a variety of experimental settings, including chemotaxis migration assays, Rac activation pull-downs, F-actin staining and immunofluorescence, and Western blot analysis of downstream effectors like PAK or cofilin. It is also well-suited for siRNA/rescue experiments and cell adhesion studies, enabling detailed investigation of DOCK2-dependent adhesion and migration. For further information or to discuss custom uses, please contact Ascent Research.
