The DPYSL5 Knockout K-562 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human chronic myeloid leukemia (CML) cell line K-562. This product provides a heterogeneous loss-of-function model with targeted disruption of the DPYSL5 gene, which encodes the collapsin response mediator protein CRMP5, a member of the CRMP family. The polyclonal nature of the knockout cells reflects the genetic diversity introduced by CRISPR/Cas9-mediated gene editing across the cell population, enabling the study of gene function without the limitations of single-cell clonal selection. No specific editing outcome is implied; rather, the population harbors a range of gene-disrupting modifications.
The K-562 cell line was originally established from the pleural effusion of a 53-year-old female with CML in blast crisis. These cells harbor the Philadelphia chromosome, resulting in the expression of the BCR-ABL1 fusion oncoprotein, and they exhibit erythroleukemic characteristics with the capacity for multipotent differentiation along erythroid, granulocytic, and monocytic lineages. K-562 is widely employed as a model system for hematopoietic cell biology, leukemia signaling, and drug resistance studies due to its well-characterized genetic background and robust growth in suspension culture.
DPYSL5 encodes CRMP5, which plays a central role in semaphorin-mediated growth cone collapse and neurite outgrowth inhibition by regulating cytoskeletal dynamics. CRMP5 is phosphorylated downstream of SEMA3A binding to the Neuropilin-1/Plexin-A1 receptor complex, a process mediated by Fyn kinase and GSK3??. Phosphorylated CRMP5 interacts directly with tubulin heterodimers and actin filaments, as well as with other CRMP family members such as CRMP1 and CRMP2, to modulate microtubule polymerization and actin reorganization. These interactions ultimately influence the activity of downstream effectors including cofilin, thereby coordinating cytoskeletal rearrangement. In cancer cells, CRMP5 has been implicated in the regulation of cell migration and invasion, suggesting a broader role in cytoskeletal signaling beyond the nervous system.
In the context of K-562 CML cells, the DPYSL5 knockout model enables the dissection of CRMP5 function within a hematopoietic malignancy background. K-562 cells possess primitive erythroid and myeloid features, and CRMP5 may contribute to processes such as adhesion, migration, and drug sensitivity that are relevant to leukemia progression. Furthermore, this model can be employed to study paraneoplastic neurological syndromes, as anti-CRMP5 autoantibodies are associated with peripheral neuropathies and cerebellar degeneration in patients with small cell lung cancer and other tumors. The polyclonal knockout population avoids clonal artifacts and is well-suited for studying population-level phenotypes in response to pharmacological inhibitors, semaphorin stimulation, or pathway modulators.
Researchers can utilize this product to investigate CRMP5 phosphorylation and protein?Cprotein interactions via Western blotting and co-immunoprecipitation, to assess changes in cell migration and invasion using transwell or wound-healing assays, and to evaluate cytotoxic or targeted therapy responses in BCR-ABL-dependent leukemia models. Additional downstream readouts include RT-qPCR for gene expression analysis, flow cytometry for surface marker profiling, and immunocytochemistry for cytoskeletal organization. The DPYSL5 Knockout K-562 Polyclonal Cells thus represent a versatile reagent for exploring CRMP5 biology in both neuronal and cancer contexts. For further information or technical support, please contact Ascent Research.
