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Cat. No. ARG34996

ACTR1B Knockout 143B Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Osteosarcoma

The ACTR1B Knockout 143B Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of 143B osteosarcoma cells with targeted disruption of the ACTR1B gene. ACTR1B is a core subunit of the dynactin Arp1 filament, essential for dynein-mediated minus-end-directed transport, mitotic spindle organization, and cell migration. It interacts with DCTN1, DCTN2, and ACTR1A, and is regulated by cell cycle kinases CDK1 and PLK1. This knockout model provides a powerful tool to dissect dynein-dynactin functions in osteosarcoma metastasis, enabling studies of organelle trafficking, migration, and mitosis. Applications include immunofluorescence, live-cell imaging, wound healing assays, and therapeutic target validation. For further details, please contact Ascent Research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    143B

    Age

    13 years

    Gene Name

    ACTR1B

    Gene Identifier

    NCBI Gene ID 10120

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM/F12

    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 ACTR1B Knockout 143B Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal population of 143B osteosarcoma cells with targeted disruption of the ACTR1B gene. ACTR1B encodes a core subunit of the dynactin Arp1 mini-filament, essential for dynein-mediated transport. The polyclonal format represents a heterogeneous pool of edited cells, providing a robust loss-of-function model without clonal selection. This population is ideal for studying dynactin-dependent processes in a bone cancer context.

The host 143B cell line is a widely used human osteosarcoma model derived from a primary tumor. Known for its highly metastatic behavior, 143B cells serve as a standard system for investigating bone cancer biology, tumor progression, and metastatic dissemination. The line’s aggressive phenotype makes it particularly suitable for evaluating genes involved in cell migration and invasion.

ACTR1B functions as a critical structural element of the dynactin complex, coupling cytoplasmic dynein to cargoes for minus-end-directed microtubule transport. Within the Arp1 filament, ACTR1B interacts with DCTN1, DCTN2, ACTR1A, and CAPZA, linking the motor to vesicles, mitochondria, and lysosomes. Upstream cell cycle kinases CDK1 and PLK1 regulate dynactin during mitosis, while downstream cargo recognition affects mitotic spindle organization and checkpoint signaling. Consequently, ACTR1B disruption impairs organelle positioning, autophagosome trafficking, and spindle assembly.

In the 143B osteosarcoma context, ACTR1B knockout provides a powerful tool to dissect contributions of dynein-dynactin to cancer cell behavior. Osteosarcoma cells depend on efficient intracellular transport and mitotic fidelity, and loss of ACTR1B is expected to impair directed cell migration??a key determinant of metastatic spread. This model enables researchers to connect dynactin complex integrity with osteosarcoma aggressiveness and to explore ACTR1B as a potential vulnerability in metastatic bone cancer.

This polyclonal knockout population enables a variety of assays, including immunofluorescence microscopy for dynactin localization, live-cell imaging of organelle transport, wound healing migration, and co-immunoprecipitation of dynactin components. Western blotting confirms ACTR1B protein loss, while flow cytometry and apoptosis assays assess cell cycle and survival effects. Applications range from mechanistic studies of mitosis and dynein cargo adaptor identification to therapeutic target validation in osteosarcoma. For further technical information or to place an order, please contact Ascent Research.

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