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Cat. No. ARG32366

BICD2 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

BICD2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human liver adenocarcinoma cell line SK-HEP-1, carrying a targeted disruption of the BICD2 gene. BICD2 encodes a dynein-dynactin adaptor that mediates retrograde Golgi-to-ER transport by linking RAB6-positive vesicles to the motor complex, and interacts with DYNC1H1, DCTN1, and GOLGA2. This model enables investigation of BICD2-dependent intracellular trafficking, Golgi organization, and cell migration in a liver cancer context. Applications include dissection of retrograde transport pathways, analysis of metastatic potential, and functional studies relevant to SMALED2 and hereditary spastic paraplegia.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    SK-HEP-1

    Sex of Donor

    Male

    Age

    52 years

    Gene Name

    BICD2

    Gene Identifier

    NCBI Gene ID 23299

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

BICD2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human liver adenocarcinoma line, harboring a targeted disruption of the BICD2 locus. This gene-edited product provides a genetically defined loss-of-function model without clonal selection, enabling investigation of BICD2-dependent retrograde trafficking and associated cellular processes in a pooled cell population.

SK-HEP-1 is an immortalized human cell line established from the ascitic fluid of a patient with liver adenocarcinoma. These cells exhibit epithelial morphology with endothelial-like features and are widely used as a model for hepatocellular carcinoma metastasis. Their robust growth and well-characterized organelle architecture facilitate analysis of intracellular trafficking dynamics.

BICD2 functions as a cargo adaptor that couples RAB6-positive vesicles to the dynein-dynactin motor complex, driving retrograde transport from the Golgi to the endoplasmic reticulum along microtubules. The protein interacts directly with the dynein heavy chain (DYNC1H1) and dynactin subunit DCTN1, as well as with Golgi-resident factors GOLGA2 and GOLGB1. Upstream, BICD2 is activated by RAB6 GTPase and regulated by cyclin-dependent kinases. It mediates COPI-independent vesicle motility and contributes to Golgi positioning, with additional interaction with PAFAH1B1 linking it to neuronal migration pathways.

In the SK-HEP-1 liver cancer context, CRISPR/Cas9-mediated BICD2 disruption is predicted to impair retrograde Golgi-to-ER trafficking, causing Golgi fragmentation and altered subcellular organization. Given the line??s metastatic potential, loss of BICD2 may compromise dynein-driven organelle transport required for efficient cell migration and invasion. Thus, this model serves to dissect the impact of trafficking defects on hepatocellular carcinoma motility and provides a relevant system to explore connections with BICD2-associated motor neuron disorders such as SMALED2 and hereditary spastic paraplegia.

The BICD2 Knockout SK-HEP-1 Polyclonal Cells enable diverse experimental applications. Knockout confirmation can be performed by Western blotting and RT-qPCR, while immunofluorescence staining for GM130 assesses Golgi morphology. Functional retrograde trafficking studies utilize RUSH-based assays or live-cell imaging. Wound-healing and transwell invasion assays quantify metastatic behavior, and co-immunoprecipitation analyses probe dynein-dynactin complex integrity. This model also supports drug screening for SMALED2 and related motor neuron diseases. For further information or to discuss custom applications, please contact Ascent Research.

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