ACTR1B Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 786-O human renal cell carcinoma line, featuring targeted disruption of the ACTR1B gene. This polyclonal knockout model provides a heterogeneous collection of cells with ACTR1B gene disruption, enabling pooled loss-of-function studies without clonal selection. The product is designed for researchers investigating dynactin complex function in cancer biology, particularly in the context of clear cell renal cell carcinoma.
The parental 786-O cell line is a widely used model of clear cell renal cell carcinoma (ccRCC). Originating from a human renal cell adenocarcinoma, these cells are VHL-null, leading to constitutive stabilization of hypoxia-inducible factor 2?? (HIF-2??), while retaining wild-type PTEN. 786-O cells exhibit an epithelial morphology and are tumorigenic, offering a genetically defined background for studying oncogenic signaling and tumor progression under hypoxic mimicry.
ACTR1B encodes the ??-subunit of the dynactin complex, an essential cofactor for cytoplasmic dynein-driven transport along microtubules. Within the dynactin complex, ACTR1B interacts directly with DCTN1/p150Glued, DCTN2/p50 dynamitin, dynein heavy chain, and Arp1 filament subunits. Through these interactions, ACTR1B facilitates dynein-mediated processes including Golgi apparatus positioning, endosomal trafficking, and mitotic spindle assembly. Expression of ACTR1B is regulated in a cell cycle-dependent manner and is influenced by HIF-2?? in hypoxic contexts typical of renal tumors, linking cytoskeletal dynamics to oncogenic hypoxia signaling.
In the VHL-deficient 786-O line, HIF-2?? stabilization creates a chronic pseudo-hypoxic state that may modulate dynactin complex dynamics. Disruption of ACTR1B in this background therefore provides a powerful tool to dissect the interplay between hypoxic signaling, cytoskeletal organization, and cell division. Since 786-O cells are motile and tumorigenic, ACTR1B knockout can reveal key mechanisms underlying renal carcinoma cell migration and metastatic potential, particularly under conditions that mimic the tumor microenvironment.
Researchers can employ ACTR1B Knockout 786-O Polyclonal Cells in a range of assays to study dynactin-dependent cellular functions. Typical applications include assessing Golgi dispersal via immunofluorescence as a readout of dynein motor activity, measuring cell motility through wound healing and transwell invasion assays, and analyzing mitotic progression by live-cell imaging and cell cycle flow cytometry. Knockout validation is readily performed using quantitative PCR and western blotting. This polyclonal model is also suitable for investigating the role of dynactin in hypoxia-adapted cancer cell behavior and for screening interventions targeting cytoskeleton-driven metastasis. For further details or technical assistance, please contact Ascent Research.
