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Cat. No. ARG35003

ACTC1 Knockout 143B Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Osteosarcoma

The ACTC1 Knockout 143B Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout model derived from the 143B human metastatic osteosarcoma cell line, with targeted disruption of the ACTC1 gene. Cardiac alpha-actin, regulated by SRF, MEF2, GATA4, and TBX5, is a core sarcomeric thin filament protein involved in actin cytoskeleton dynamics. These cells enable functional studies of cell motility, sarcomere protein interactions, and drug screening for cardiomyopathies and cancer. Representative assays include western blotting, phalloidin staining, and transwell invasion. ACTC1 interacts with tropomyosin, troponin complex, and myosin heavy chain, linking the model to cardiac muscle contraction and actin signaling 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

    ACTC1

    Gene Identifier

    NCBI Gene ID 70

    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 ACTC1 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the 143B human osteosarcoma cell line, featuring targeted disruption of the ACTC1 locus. This polyclonal pool retains genetic heterogeneity while achieving loss of gene function, enabling robust and unbiased functional analyses in a cell population context.

The 143B cell line is a well-characterized, thymidine kinase-deficient (TK-) human osteosarcoma model with high metastatic potential. Derived from the HOS cell line, 143B is extensively utilized to study tumor cell migration, invasion, and metastasis. Its TK- status facilitates selection in HAT medium, and its well-documented signaling networks and adherent growth make it an ideal host for CRISPR-based gene editing and downstream phenotypic assays.

ACTC1 encodes cardiac alpha-actin, a major constituent of the sarcomeric thin filament required for cardiac muscle contraction. Transcription is regulated by the cardiac transcription factors SRF, MEF2, GATA4, and TBX5. The protein assembles into F-actin and directly interacts with tropomyosin, the troponin complex (troponin T, I, C), myosin heavy chain, alpha-actinin, and nebulin to orchestrate sarcomere organization. This network includes pathway components ACTC1, MYH6, TNNT2, TPM1, and TTN. Beyond its sarcomeric role, ACTC1 modulates actin cytoskeleton signaling, affecting cell shape, adhesion, and motility.

In the 143B metastatic osteosarcoma background, ACTC1 knockout establishes a unique system for exploring non-canonical functions of cardiac actin in a mesenchymal cancer context. The model enables dissection of how sarcomeric actin isoforms influence actin cytoskeleton dynamics, cell adhesion, and migration??processes central to cancer cell dissemination. It also offers a simplified cellular platform to study the pathological consequences of ACTC1 dysregulation observed in dilated cardiomyopathy, hypertrophic cardiomyopathy, atrial septal defects, and congenital heart defects.

This polyclonal knockout cell product is suitable for a wide array of applications. Researchers can assess protein expression via western blotting, visualize F-actin structures with phalloidin staining or immunocytochemistry, and measure cell migration and invasion with wound healing and transwell assays, as well as proliferation rates. The cells are valuable for drug screening campaigns targeting actin-mediated pathways relevant to both cardiomyopathies and cancer metastasis. For further inquiries, please contact Ascent Research.

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