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Cat. No. ARG35286

ACTC1 Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

The ACTC1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the AGS human gastric epithelial cell line, featuring disruption of the ACTC1 gene. Alpha-cardiac actin, the encoded protein, is essential for sarcomeric thin filament formation and cytoskeletal organization. This model enables investigation of ACTC1's roles in actin dynamics, cell adhesion, and migration within a gastric cancer context. ACTC1 is transcriptionally activated by SRF and MEF2 and interacts with tropomyosin and myosin to control contractility. Key applications include cardiomyopathy disease modeling, cardiac drug screening, and gastric cancer cell motility studies using assays such as western blotting, immunofluorescence, and migration/invasion assays.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    AGS

    Sex of Donor

    Female

    Age

    54 years

    Derived From Site

    In situ; Stomach

    Gene Name

    ACTC1

    Gene Identifier

    NCBI Gene ID 70

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    Ham's F-12

    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

ACTC1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of AGS human gastric epithelial cells, designed for disruption of the ACTC1 gene. Alpha-cardiac actin, the encoded protein, is a major sarcomeric thin filament component essential for cardiac muscle contraction and cytoskeletal integrity. This heterogeneous cell pool enables unbiased loss-of-function studies, avoiding clonal selection bias, and is well-suited for pooled genetic screens and population-level phenotypic assays.

The AGS cell line, derived from a primary tumor of a gastric cancer patient, is a widely employed epithelial model for gastric cancer research, including proliferation, migration, and oncogenic signaling studies. The engineering of ACTC1 knockout in this background creates a unique tool to dissect the non-canonical functions of cardiac actin in cytoskeletal organization and cell motility.

ACTC1 is transcriptionally regulated by SRF, MEF2, GATA4, and Myocardin, linking extracellular signals to actin filament assembly. It polymerizes into F-actin and interacts with myosin heavy chain, tropomyosin, troponin, and alpha-actinin to mediate actomyosin contractility and sarcomere assembly. Disruption impairs these interactions, reducing cytoskeletal tension. ACTC1 functions upstream of RhoA and ACTB, and its loss can disrupt focal adhesion and tight junction integrity. Key co-analyzed pathway components include MYH6, TNNT2, and MYL2.

In the AGS gastric cancer background, ACTC1 knockout serves as a powerful tool to examine how loss of cardiac actin remodels epithelial cell behavior. Disruption of ACTC1-driven actin polymerization alters cell adhesion dynamics, impairs focal adhesion turnover, and modulates migration and invasion through Rho GTPase signaling. This model is particularly relevant for elucidating actin isoform-specific mechanisms in gastric cancer metastasis. Furthermore, due to conserved actin biology, these cells can be employed in cardiomyopathy research for drug screening and mechanistic studies of sarcomeric protein function.

The ACTC1 Knockout AGS Polyclonal Cells support diverse research applications, including cardiomyopathy disease modeling, cardiac drug screening, and actin isoform functional comparisons. Gastric cancer motility studies utilize wound healing and Matrigel invasion assays. Protein-level changes are confirmed by Western blotting for ACTC1 and sarcomeric proteins or co-immunoprecipitation of actin-binding partners such as tropomyosin and alpha-actinin. Immunofluorescence visualizes F-actin organization and focal adhesion integrity, while qPCR quantifies transcription of cardiac genes and downstream targets. For additional details or to inquire about this product, please contact Ascent Research.

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