The DOCK7 Knockout K-562 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human chronic myelogenous leukemia (CML) cell line K-562. This product offers a heterogeneous pool of cells harboring targeted disruption of the DOCK7 gene, enabling comprehensive loss-of-function analysis without the biases introduced by clonal selection. The polyclonal format ensures a broad representation of editing events, providing a robust model for functional genomics studies.
K-562 cells were originally established from the pleural effusion of a CML patient in blast crisis and are characterized by the presence of the Philadelphia chromosome, which generates the BCR-ABL1 fusion oncogene. As multipotent hematopoietic progenitor cells, K-562 cells exhibit the potential to differentiate along erythroid, granulocytic, and monocytic pathways, making them a favored system for investigating hematopoietic signaling, leukemogenesis, and therapeutic resistance. Their rapid proliferation and well-defined signaling networks further enhance their utility as a host for genetic perturbation.
DOCK7 functions as a guanine nucleotide exchange factor (GEF) that specifically activates the small GTPases Rac1 and Cdc42. The protein is regulated upstream by PI3K, growth factor receptors, and TACC3, and it physically interacts with TACC3, Rac1, and Cdc42. Upon activation, DOCK7 catalyzes the exchange of GDP for GTP on Rac1 and Cdc42, triggering downstream effectors including PAK and JNK kinases and culminating in actin cytoskeleton reorganization. This signaling cascade governs essential processes such as cell migration, adhesion, and neuronal development, and genetic disruption of DOCK7 provides a direct means to interrogate these pathways.
Within the K-562 leukemic background, DOCK7-mediated Rac1/Cdc42 signaling is likely involved in regulating cytoskeletal dynamics that influence cell adhesion, migration, and perhaps the differentiation capacity of these multipotent progenitors. Knockout of DOCK7 in these cells enables the dissection of how this GEF contributes to BCR-ABL1-driven oncogenic signaling and may reveal vulnerabilities related to cytoskeletal control. Moreover, the polyclonal population avoids the potential artifacts of single-cell cloning and better mirrors the cellular heterogeneity encountered in clinical samples.
This knockout model is suited for a wide array of experimental applications. Researchers can validate DOCK7 depletion by Western blotting or RT-qPCR, assess Rac1 and Cdc42 activation levels using G-LISA or pull-down assays, and visualize actin cytoskeletal structures via immunofluorescence. Functional studies may include cell migration and invasion assays, flow cytometric analysis of adhesion molecules, and phospho-signaling profiling of PAK and JNK. Additionally, the cells can be used in drug sensitivity testing with BCR-ABL inhibitors to explore resistance mechanisms. For additional information and customization options, please contact Ascent Research.
