DST Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human K-562 leukemia cell line, engineered for targeted disruption of the DST gene. This product provides a loss-of-function model to investigate dystonin-mediated cytoskeletal organization and associated signaling networks.
The K-562 host cell line was established from the pleural effusion of a 53-year-old female with chronic myeloid leukemia in blast crisis and carries the Philadelphia chromosome (BCR-ABL1 fusion). Widely used as a model for hematopoietic differentiation and leukemia biology, K-562 cells grow in suspension and exhibit lymphoblast morphology. Their well-characterized signaling landscape and ease of genetic manipulation make them a robust platform for studying gene function in a leukemic context.
The DST gene encodes dystonin, a large cytoskeletal linker protein that mechanically integrates intermediate filaments with actin and microtubules. Dystonin is critical for hemidesmosome assembly, intermediate filament organization, and cell-matrix adhesion. Its activity is regulated by upstream signals such as integrin-??1, TGF-??, and the transcription factor p63. Dystonin directly interacts with keratin intermediate filaments, plectin, BPAG2 (collagen type XVII), tubulin, and actin to stabilize the cytoskeletal network. Through these interactions, DST contributes to focal adhesion dynamics and cell migration, functioning downstream of integrin ??6??4 and laminin-332 in epithelial adhesion complexes.
In the K-562 leukemic background, disruption of DST is expected to perturb cytoskeletal architecture, potentially altering cell shape, adhesion properties, and migration capacity even in a suspension cell model. Given that dystonin interfaces with integrin signaling and focal adhesion components, its loss may modulate BCR-ABL1-dependent pathways and influence leukemic cell behavior. This polyclonal knockout population therefore serves as a valuable tool to explore crosstalk between cytoskeletal integrity and oncogenic signaling in chronic myeloid leukemia.
Researchers can employ this DST knockout model to investigate cytoskeletal reorganization, cell adhesion, and migration in hematopoietic malignancies, as well as to dissect the role of dystonin in drug responsiveness and apoptosis. Compatible assays include western blotting and RT-qPCR for expression analysis, immunofluorescence and flow cytometry for spatial and quantitative protein assessment, cell adhesion and apoptosis assays for functional readouts, and RNA-seq for global transcriptome profiling. For additional information or custom requests, please contact Ascent Research.
