ACTR1B Knockout DLD-1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human DLD-1 colorectal adenocarcinoma cell line. This loss-of-function model targets the ACTR1B gene, enabling investigation of the dynactin complex and dynein-mediated intracellular transport. The polyclonal nature preserves genetic heterogeneity while eliminating functional ACTR1B, facilitating robust functional studies in a cancer context.
The DLD-1 cell line is an extensively characterized human epithelial colorectal adenocarcinoma model, harboring mutations in APC and KRAS and exhibiting chromosomal instability. Widely used in cancer biology, these adherent cells are ideal for imaging-based assays of intracellular transport, mitotic progression, and signal transduction, with direct relevance to colorectal tumorigenesis.
ACTR1B encodes a core subunit of the dynactin complex, an essential cofactor for cytoplasmic dynein motor activity. ACTR1B interacts directly with DCTN1/p150Glued, DCTN2/p50, ACTR1A, and the dynein heavy chain, connecting dynein to cargos via adaptors like BICD2. This structural role is critical for dynein processivity and minus-end-directed transport along microtubules. Knockout disrupts dynein-mediated processes including mitotic spindle assembly, endosomal?Clysosomal trafficking, and Golgi positioning. Upstream, the gene is regulated by E2F transcription factors, MYC, and Rho GTPases, placing ACTR1B at a nexus of cell cycle control and motor-dependent trafficking.
Within the DLD-1 colorectal cancer context, ACTR1B knockout is particularly valuable for dissecting transport-dependent mechanisms of tumor progression. Colorectal cancer cells rely on precise organelle positioning and vesicle trafficking for proliferation and invasion. The polyclonal knockout population mirrors tumor heterogeneity, permitting analysis of dynactin dysfunction on mitotic fidelity and intracellular logistics.
Researchers can apply this model to diverse assays: western blotting and immunofluorescence for ACTR1B and organelle markers; live-cell imaging of vesicle motility; mitotic spindle analysis by confocal microscopy; cell cycle flow cytometry; and co-immunoprecipitation of dynactin components. These approaches support investigations of colorectal cancer progression, dynactin-related neurodegenerative disorders, and drug target screening for transport-based therapies. For additional details, contact Ascent Research.
