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Cat. No. ARG32757

KIF16B Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

The KIF16B Knockout SK-HEP-1 Polyclonal Cells provide a CRISPR/Cas9-edited loss-of-function model of the endosomal kinesin KIF16B in a human liver adenocarcinoma cell line. This polyclonal knockout population disrupts KIF16B, a motor protein that binds PI3P and mediates early endosome trafficking and EGFR recycling, ultimately regulating AKT signaling and cell migration. Engineered on the tumorigenic SK-HEP-1 background, the model is optimized for studying endocytosis-dependent EGFR signaling, drug resistance, and metastasis in hepatocellular carcinoma. Representative applications include Western blotting, endocytosis assays, immunofluorescence, and migration assays, enabling detailed dissection of trafficking-related cancer pathways.

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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

    KIF16B

    Gene Identifier

    NCBI Gene ID 55614

    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 KIF16B Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of SK-HEP-1 liver adenocarcinoma cells carrying a disrupted KIF16B gene. This model facilitates loss-of-function studies without clonal isolation, providing a robust genetic background for analyzing KIF16B-dependent phenotypes.

SK-HEP-1 is a tumorigenic human hepatic adenocarcinoma cell line derived from the ascites of a 52-year-old male patient. Known for its epithelial morphology and reliability in liver cancer research, this line retains active EGFR and PI3K/AKT signaling pathways, making it highly suitable for investigations of receptor trafficking and tumor cell biology.

KIF16B is a plus-end-directed kinesin motor that binds phosphatidylinositol 3-phosphate (PI3P) on early endosomes, driving their microtubule-dependent transport. Regulated by the small GTPase Rab5, KIF16B collaborates with sorting nexins (SNX) and the dynein-dynactin complex to sort internalized receptors, including EGFR, for recycling to the plasma membrane. By facilitating efficient EGFR recycling, KIF16B sustains downstream AKT signaling; its disruption attenuates AKT phosphorylation and alters cell migration and proliferation.

In SK-HEP-1 cells, KIF16B knockout impairs the spatial control of EGFR, thereby reducing AKT pathway activity. This disruption provides a powerful model to study endosomal regulation of oncogenic signaling in liver cancer, with direct relevance to mechanisms of EGFR-driven proliferation, drug resistance, and metastatic behavior. The polyclonal editing strategy avoids artifacts from clonal selection while maintaining a predominantly KIF16B-null background.

Applications include Western blot analysis of EGFR and phospho-AKT (Ser473), transferrin-based endocytosis assays, immunofluorescence staining for EEA1 and Rab5, scratch wound migration assays, and cell proliferation measurements. The model is ideally suited for exploring endocytic trafficking??s role in liver cancer drug resistance and metastasis. For inquiries, contact Ascent Research.

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