The DPYSL2 Knockout K-562 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the DPYSL2 gene has been disrupted. This gene encodes collapsin response mediator protein 2 (CRMP2), a microtubule-associated protein with roles in cytoskeletal reorganization. The polyclonal knockout format provides a mixed population of DPYSL2 loss-of-function cells, enabling robust functional studies without clonal isolation. It is designed for researchers investigating DPYSL2-dependent mechanisms in hematopoietic malignancy and neural-related signaling within a leukemia context.
The knockout was generated in the K-562 human chronic myeloid leukemia (CML) cell line, derived from a patient in blast crisis. K-562 cells are BCR-ABL-positive and exhibit an undifferentiated blast phenotype, widely used as a model for hematopoietic differentiation and leukemia biology. Their genetic background and rapid proliferation suit them for dissecting oncogenic signaling and testing targeted therapies, providing a relevant context to study DPYSL2 function in a leukemic milieu.
DPYSL2/CRMP2 mediates semaphorin 3A (Sema3A) signaling downstream of plexin-A1 and neuropilin-1 receptors. Its activity is controlled by phosphorylation through Cdk5, GSK3??, and Rho kinase (ROCK). CRMP2 interacts with tubulin heterodimers to promote microtubule assembly and with actin filaments to coordinate cytoskeletal dynamics, regulating cell polarity, migration, and trafficking. It also interfaces with CRMP family members (DPYSL3, DPYSL4, DPYSL5) to modulate microtubule stability. Disruption of DPYSL2 uncouples these processes, offering a loss-of-function model to deconvolute CRMP2 signaling nodes.
In K-562 leukemia cells, DPYSL2 knockout likely perturbs proliferation-apoptosis balance, as CRMP2 is implicated in cell cycle progression and survival. Given cytoskeletal remodeling’s role in division and migration, this model enables study of microtubule dynamics on BCR-ABL-driven oncogenesis. Researchers can assess if CRMP2 deficiency alters sensitivity to tyrosine kinase inhibitors. The model also provides insights into neural guidance cues in hematopoietic malignancy, as semaphorin components may contribute to niche interactions.
The DPYSL2 Knockout K-562 Polyclonal Cells support functional assays including Western blotting for DPYSL2 and downstream targets, immunofluorescence for cytoskeletal architecture, Boyden chamber migration assays, MTS/MTT proliferation assays, and flow cytometry for apoptosis (Annexin V/PI). Phospho-CRMP2 analysis reports upstream kinase activity. These cells facilitate drug target validation and mechanistic studies in leukemia biology. For more information, please contact Ascent Research.
