The DOCK5 Knockout K-562 Polyclonal Cells constitute a polyclonal human knockout cell population generated by CRISPR/Cas9-mediated disruption of DOCK5 in the K-562 cell line. The heterogeneous pool includes cells with distinct loss-of-function alleles, avoiding clonal selection artifacts. This format is ideal for pooled screening, bulk biochemical assays, and population-level phenotypic analysis, all while retaining the scalable suspension growth properties of K-562 cells.
The K-562 host line is a BCR-ABL-positive human leukemic lymphoblast model derived from a blast crisis patient. These cells grow in suspension and are widely applied in CML research, hematopoietic differentiation studies, and drug resistance screening. K-562 cells express constitutively active BCR-ABL tyrosine kinase, making them a standard system for evaluating tyrosine kinase inhibitors such as imatinib. Their robust suspension culture facilitates high-throughput and large-scale experimental workflows.
DOCK5 encodes a GEF that activates RAC1 and CDC42 through its DHR-2 domain, forming a complex with ELMO1/ELMO2. Activated RAC1/CDC42 stimulate PAK1 and WAVE2, leading to ARP2/3-dependent actin polymerization, lamellipodia formation, and cell migration. Upstream, DOCK5 is regulated by BCR-ABL signaling, integrins, and receptor tyrosine kinases such as PDGFR and EGFR. NCK1 is an additional interacting partner that modulates DOCK5 activity.
In K-562 leukemia cells, DOCK5-mediated cytoskeletal remodeling is implicated in migration, invasion, and drug resistance. BCR-ABL-driven cytoskeletal dysregulation may converge on DOCK5; its disruption therefore offers a loss-of-function model to dissect RAC1/CDC42-dependent processes and their impact on leukemic cell behavior. This model is valuable for studying how DOCK5 contributes to imatinib sensitivity and for exploring anti-metastatic strategies.
Applications include Boyden chamber migration and invasion assays, confocal F-actin imaging, G-LISA-based RAC1/CDC42 activity measurements, Western blotting for DOCK5 and downstream effectors, and co-immunoprecipitation of DOCK5-ELMO complexes. Proliferation and imatinib sensitivity profiling can be conducted, and the cells are amenable to pooled functional genomics screens. For further details, please contact Ascent Research.
