The CD2AP Knockout K-562 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population of the human chronic myelogenous leukemia (CML) cell line K-562, engineered for loss-of-function studies of the adaptor protein CD2AP. This polyclonal knockout cell product consists of a heterogeneous population of K-562 cells harboring distinct CRISPR/Cas9-mediated disruptions in the CD2AP gene, enabling robust investigation of gene function without single-cell cloning artifacts.
The parental K-562 cell line was derived from a 53-year-old female with CML in blast crisis and is characterized by the presence of the BCR-ABL fusion oncogene. As a pluripotent hematopoietic malignancy model, K-562 cells serve as a widely used system for studying CML signal transduction, drug response, and leukemogenesis. The line retains features of multipotent progenitor cells and is responsive to a range of cytokines and chemical perturbations, making it a versatile platform for genetic manipulation and pathway analysis.
CD2AP encodes an adaptor protein that bridges membrane receptors, including CD2 and nephrin, to the actin cytoskeleton through direct interactions with cortactin, CAPZ, and the Arp2/3 complex. It functions as a scaffold in multiple signaling cascades, linking receptor activation to downstream effectors such as Akt, PI3K, Rac1, and MAP kinases. CD2AP participates in the formation of the nephrin-CD2AP complex, the PDGFR-CD2AP-p130Cas axis, and the TCR-CD2AP-WASP pathway, thereby regulating endocytosis, cell adhesion, and dynamic actin polymerization. Upstream regulators include PDGF, TGF-??, and T-cell receptor activation, while CD2AP interacts with c-Cbl, p130Cas, Fyn, and ALIX to coordinate signal transduction and cytoskeletal remodeling.
Knockout of CD2AP in K-562 cells is predicted to disrupt scaffolding functions that integrate membrane-proximal signals with cytoskeletal organization. In the BCR-ABL-driven context, loss of CD2AP may alter proliferative signaling, cell migration, and survival responses, offering a unique tool to dissect intersection points between oncogenic kinase signaling and actin-dependent processes. This model enables the study of how adaptor proteins modulate leukemia cell behavior and potentially contribute to drug resistance mechanisms.
Key applications include probing CD2AP-related pathways in leukemic signal transduction, investigating roles in cell adhesion and migration as they relate to cancer metastasis, and performing protein?Cprotein interaction studies via co-immunoprecipitation of known interactors such as c-Cbl and Fyn. Downstream signaling output can be assessed by Western blotting for phospho-Akt, phospho-MAP kinase, or Rac1 activation, while functional consequences on proliferation and migration are evaluated using standard cell-based assays. Flow cytometry further enables monitoring of surface marker expression changes upon CD2AP disruption. This polyclonal knockout population provides a ready-to-use, physiologically relevant system for dissecting adaptor protein function in a well-characterized leukemic background. For additional product details and technical support, please contact Ascent Research.
