This product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human BICD1 gene in SK-HEP-1 cells. The polyclonal pool carries heterogeneous disruptions of the BICD1 locus via non-homologous end joining, enabling loss-of-function studies without single-cell clonal selection. This format preserves population-level diversity while abrogating BICD1 protein expression, providing a versatile tool for investigating dynein-based retrograde transport.
The host cell line SK-HEP-1 originated from the ascites of a patient with liver adenocarcinoma and is widely used as a model for hepatocellular carcinoma and endothelial biology. Its dual mesenchymal and endothelial characteristics make it suitable for studying tumor cell plasticity, angiogenesis, and metastasis. The cell line??s well-characterized genomic landscape and adaptability to standard culture conditions facilitate robust experimental manipulations and screening campaigns.
BICD1 encodes a coiled-coil adaptor protein that bridges the dynein?Cdynactin motor complex to Rab6-positive vesicles, orchestrating their microtubule minus-end-directed transport. It directly interacts with DYNC1H1 (dynein heavy chain), DCTN1 (p150Glued), RAB6A, and the nucleoporin RANBP2. Through these associations, BICD1 governs retrograde trafficking of cargo from the Golgi apparatus to the endoplasmic reticulum and positions the Golgi around the centrosome. BICD1 thus acts downstream of RAB6A activation and upstream of dynein motor recruitment, coordinating organelle distribution and intracellular logistics essential for polarized secretion and cell migration.
In the SK-HEP-1 liver cancer context, disruption of BICD1-mediated transport is expected to perturb Golgi organization and vesicular cargo flow, processes frequently dysregulated during malignant progression. Loss of BICD1 function can impair dynein-dependent positioning of the Golgi, potentially altering polarized protein secretion, cell adhesion, and directional migration??phenotypes linked to hepatocellular carcinoma invasion and metastasis. This knockout model therefore provides a relevant platform to dissect how retrograde transport contributes to tumor cell pathophysiology.
This polyclonal knockout population supports diverse applications: western blotting and immunofluorescence for Golgi markers (GM130, giantin) to validate Golgi dispersal; live-cell imaging to monitor vesicular trafficking; wound-healing assays to assess migration; co-immunoprecipitation with dynein; and RNA-seq for transcriptome profiling. These tools enable studies of dynein cargo specificity, Golgi positioning in hepatocellular carcinoma, and drug screening for motor protein modulators. For further technical details, please contact Ascent Research.
