The DNM3 Knockout K-562 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the DNM3 gene in the K-562 chronic myelogenous leukemia (CML) cell line. This loss-of-function model enables researchers to study the cellular consequences of DNM3 depletion in a hematopoietic progenitor-like background.
K-562 cells were originally established from the pleural effusion of a 53-year-old female with CML in blast crisis and are characterized by the presence of the BCR-ABL1 fusion oncogene. These cells serve as a widely employed model for investigating erythroid differentiation, leukemia biology, and signal transduction pathways. Their suspension growth and robust responsiveness to stimuli make them particularly suitable for endocytosis and receptor trafficking studies.
DNM3 encodes a dynamin-family GTPase that catalyzes membrane fission during clathrin-mediated endocytosis and synaptic vesicle recycling. This protein is activated downstream of epidermal growth factor (EGF) receptor signaling and is regulated by upstream factors including calcium influx, SRC kinases, and the RAB5 GTPase. It interacts with BAR domain-containing proteins such as amphiphysin and endophilin, as well as actin regulatory factors including cortactin, N-WASP, and Abp1. Upon GTP hydrolysis, DNM3 constricts the necks of invaginating clathrin-coated vesicles, leading to scission and vesicle release. Additionally, DNM3 participates in the regulation of actin dynamics and focal adhesion remodeling, processes critical for cell migration and invasion.
In the context of K-562 cells, disruption of DNM3 is expected to impair constitutive and ligand-induced endocytosis, thereby altering the surface expression and signaling of receptors such as transferrin receptor and EGFR. This can perturb downstream pathways dependent on endocytic trafficking, including the mitogen-activated protein kinase (MAPK) cascade, and may modulate actin cytoskeleton organization. Because K-562 cells are used to model aspects of leukemia pathology, the DNM3 knockout provides a platform to examine how dynamin-mediated membrane remodeling influences cancer cell behavior, including proliferation, migration, and response to chemotherapeutic agents.
Typical research applications include analyzing endocytic uptake dynamics via transferrin internalization assays, evaluating receptor-mediated signaling through phosphoproteomic analyses, and assessing cell migration capacity using transwell assays. This model is also suitable for flow cytometric quantification of surface receptor levels, immunofluorescence visualization of clathrin and actin structures, and transcriptional profiling via RNA-seq. Additionally, it can be employed in genetic interaction screens and to investigate the role of endocytosis in drug sensitivity. For further information, including batch-specific validation data and technical support, please contact Ascent Research.
