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Cat. No. ARG32268

ARMC9 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

The ARMC9 Knockout SK-HEP-1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal ARMC9 knockout in the SK-HEP-1 liver adenocarcinoma cell line, which exhibits endothelial-like characteristics. This loss-of-function model enables investigation of ciliary protein ARMC9 in hepatic adenocarcinoma research. ARMC9 functions in intraflagellar transport and modulates Wnt/??-catenin signaling via interactions with IFT20, IFT88, and KIF3B, affecting ??-catenin downstream of Wnt3a/Frizzled. Knockout impairs ciliogenesis and Wnt activity, facilitating studies on ciliopathies, Joubert syndrome, and hepatocellular carcinoma. Applications include Western blot, immunofluorescence, Wnt reporter, and drug screening assays.

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Shipping Info:

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

    ARMC9

    Gene Identifier

    NCBI Gene ID 80210

    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

The ARMC9 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population for loss-of-function studies of ARMC9. The polyclonal format minimizes clonal artifacts, ensuring a representative genetic background. Supplied as a ready-to-use pool, this knockout model is suited for diverse assays including signaling analysis, ciliary assessment, and drug screening in hepatic adenocarcinoma research.

The SK-HEP-1 host cell line was established from ascites of a liver adenocarcinoma patient and exhibits endothelial-like features alongside its epithelial origin, making it a valuable model for investigating tumor biology, angiogenesis, and epithelial-mesenchymal transitions. These cells are extensively utilized in hepatocellular carcinoma research for proliferation, migration, invasion, and drug response studies, and provide a robust background for gene editing.

ARMC9 is a ciliary protein critical for intraflagellar transport (IFT), interacting with IFT20, IFT88, and KIF3B, and integrating into IFT-A/B complexes and the BBSome. Its expression is regulated by RFX transcription factors and Notch signaling. ARMC9 modulates Wnt/??-catenin signaling downstream of Wnt3a and Frizzled, affecting ??-catenin stability. Knockout thus impairs ciliogenesis and attenuates Wnt pathway activity.

In SK-HEP-1 cells, ARMC9 disruption compromises primary cilium formation and intraflagellar transport, leading to altered Wnt/??-catenin signaling that may influence proliferation and differentiation. Given the established links between ciliary dysfunction and liver tumorigenesis, this model is highly relevant for dissecting hepatocellular carcinoma mechanisms and ciliopathies such as Joubert syndrome, particularly the role of ??-catenin dysregulation. It also serves as a platform for drug screening targeting ciliopathy-related hepatic cancers.

This polyclonal knockout pool supports multiple applications: Western blot and RT-qPCR for knockout confirmation; immunofluorescence with acetylated ??-tubulin or Arl13b to assess ciliary integrity; TOP/FOP flash reporter assays for Wnt pathway activity; MTT proliferation, migration, and invasion assays; and RNA-seq for transcriptomic profiling. It enables detailed mechanistic studies and drug screening targeting ciliary and Wnt signaling in hepatic adenocarcinoma. For further information, contact Ascent Research.

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