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Cat. No. ARG32732

KATNA1 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

This CRISPR/Cas9-edited polyclonal KATNA1 knockout cell population, derived from the SK-HEP-1 liver adenocarcinoma line, disrupts the p60 katanin subunit critical for microtubule severing. KATNA1 is activated by Aurora A and PLK1 kinases and partners with the p80 subunit (KATNB1) to regulate spindle assembly, cilium dynamics, and YAP/TAZ signaling. The model enables investigation of katanin-dependent processes in hepatocellular carcinoma, including mitotic regulation, migration, and invasion. Applications include live-cell imaging, immunofluorescence, flow cytometry, and drug sensitivity assays, making it a valuable tool for cancer cell biology and cytoskeletal research.

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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

    KATNA1

    Gene Identifier

    NCBI Gene ID 11104

    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

KATNA1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the SK-HEP-1 human liver adenocarcinoma cell line. This product contains a pool of cells with targeted disruption of the KATNA1 gene, leading to loss of the p60 katanin catalytic subunit. As a polyclonal knockout model, it enables bulk population analyses without single-cell clone isolation, making it suitable for studying KATNA1-dependent microtubule-severing and its roles in mitotic progression and hepatocellular carcinoma.

The SK-HEP-1 host cell line originated from ascitic fluid of a 52-year-old male with liver adenocarcinoma and exhibits an epithelial-like, mesenchymal phenotype. Although sometimes considered of endothelial origin, SK-HEP-1 is widely used as a hepatocellular carcinoma model due to its tumorigenic and metastatic properties. The KATNA1 knockout in this background provides a relevant system to examine how katanin dysfunction influences liver cancer cell biology, including migration, invasion, and drug response.

KATNA1 encodes the catalytic p60 subunit of katanin, a microtubule-severing AAA ATPase. The p60 subunit is phosphorylated and activated by Aurora A kinase (AURKA) and Polo-like kinase 1 (PLK1), and is recruited to microtubules by the p80 subunit KATNB1. Katanin severs microtubules to orchestrate mitotic spindle assembly, centrosome separation, cilium disassembly, and axon branching. Additional regulators include Spastin, NDEL1, and EML1, while downstream effects involve YAP/TAZ cytosolic retention. Dysregulation of this network contributes to microcephaly, Seckel syndrome, and cancer.

In liver adenocarcinoma SK-HEP-1 cells, KATNA1 knockout permits dissection of microtubule-severing roles in proliferation, spindle checkpoint control, and sensitivity to microtubule-targeting chemotherapeutics. The model is especially useful for studying metastasis, as dynamic microtubule reorganization is essential for cell migration and invasion. Thus, these cells offer a platform to investigate KATNA1 as a potential therapeutic vulnerability in hepatocellular carcinoma.

Applications include live-cell imaging of spindle dynamics, immunofluorescence staining for ??-tubulin and ??-tubulin, and flow cytometry-based cell cycle analysis. These polyclonal cells are also suited for wound healing, Transwell migration, and spheroid invasion assays to probe motility and invasion. Co-immunoprecipitation can verify KATNA1-KATNB1 interactions, and drug sensitivity screens can assess cytotoxic responses. Expression changes can be monitored by RT-qPCR and Western blotting. For further information, please contact Ascent Research.

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