The EHD3 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the K-562 chronic myeloid leukemia cell line, generated for targeted disruption of the EHD3 gene (EH domain-containing protein 3). This heterogeneous product pool comprises a diverse array of gene-edited cells, each harboring unique loss-of-function alleles, and is ideally suited for functional genomics studies investigating the role of EHD3 in membrane trafficking within a leukemic background. The polyclonal format minimizes clonal bias while enabling robust analysis of trafficking-dependent phenotypes.
The K-562 host cell line was originally established from a pleural effusion of a patient with chronic myeloid leukemia in blast crisis. These suspension-adapted cells exhibit features of undifferentiated hematopoietic progenitors and serve as a well-characterized model for studying myeloid leukemia biology, signal transduction, and therapeutic responses. Their rapid growth and genetic tractability make them a popular choice for CRISPR-based editing and high-throughput screening.
EHD3 functions as a critical mediator of endosomal membrane remodeling, orchestrating receptor recycling from early endosomes back to the plasma membrane. It is activated downstream of cytokine and growth factor stimulation, with the PI3K/AKT pathway providing regulatory input. EHD3 interacts with Rab11-FIP2, Arf6, Pacsin2, and Syndapin2 to form membrane-remodeling complexes that facilitate the transport of receptors such as the transferrin receptor (TFRC), ??1-integrin, and the epidermal growth factor receptor (EGFR). This recycling process directly controls surface receptor abundance, thereby modulating cellular responses including adhesion, migration, and proliferation.
In the K-562 leukemia context, EHD3-mediated receptor trafficking is particularly relevant to oncogenic signaling. Dysregulation of endocytic pathways has been linked to aberrant survival and drug resistance in acute and chronic myeloid leukemias. By disrupting EHD3 in these cells, researchers can dissect how altered recycling of ??1-integrins and growth factor receptors impacts leukemic cell adhesion, migration, and sensitivity to tyrosine kinase inhibitors, providing insights into potential therapeutic vulnerabilities.
This polyclonal knockout product supports a wide range of experimental applications. Researchers can employ flow cytometry to quantify surface TFRC levels, perform transferrin uptake assays to assess recycling kinetics, and conduct cell migration and proliferation assays to evaluate functional consequences. Combined with Western blotting and RT-qPCR to verify target disruption, the cells offer a comprehensive platform for studying EHD3-dependent trafficking in myeloid leukemia. For further information or technical support, please contact Ascent Research.
