The EHD1 Knockout K-562 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the K-562 human chronic myelogenous leukemia cell line. This population carries a targeted disruption of the EHD1 gene, generating a loss-of-function model for studying endocytic recycling and membrane trafficking processes. The polyclonal format provides a heterogeneous knockout cell pool suitable for functional studies without single-cell cloning bottlenecks.
The K-562 cell line was established from the pleural effusion of a patient with chronic myelogenous leukemia in blast crisis and is characterized by expression of the BCR-ABL fusion oncoprotein. Widely used as a model for hematopoietic differentiation and leukemia biology, K-562 cells exhibit erythroid and myeloid progenitors amenable to differentiation studies. Their robust growth and well-defined signaling landscape make them an ideal host for gene-editing applications in cancer and hematopoietic cell biology.
EHD1 encodes an ATPase that oligomerizes and remodels membranes to drive fission of recycling endosomes, thereby controlling the return of internalized receptors and integrins to the plasma membrane. EHD1 functions downstream of EGF and Rab11 signaling and interacts with key effectors such as Rab11-FIP2, MICAL-L1, and Arf6 to orchestrate endocytic recycling. Its activity directly regulates the surface levels of transferrin receptor, ??1 integrin, and EGFR, and contributes to actin cytoskeletal remodeling essential for cell adhesion, migration, and signaling modulation. By coupling receptor recycling with membrane organization, EHD1 integrates growth factor responses with integrin-mediated adhesion pathways.
Disruption of EHD1 in K-562 cells provides a unique tool for examining how endocytic trafficking intersects with leukemogenic signaling and hematopoietic phenotypes. Loss of EHD1 disrupts the recycling of key surface proteins, potentially impairing integrin-dependent adhesion and EGFR-driven proliferation, and may alter the migratory and invasive properties critical in blast crisis progression. This knockout model thus allows dissection of BCR-ABL-dependent and independent trafficking mechanisms in a hematological malignancy context.
Researchers can employ this polyclonal knockout population in assays measuring transferrin and integrin recycling kinetics, surface biotinylation-based recycling analyses, quantitative imaging of endosome dynamics, and cell migration/invasion studies. Flow cytometry and western blotting enable assessment of surface receptor and signaling molecule levels, aiding in the elucidation of EHD1??s role in cancer cell biology, developmental disorders, and neurological disease mechanisms. For further information, please contact Ascent Research.
