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Cat. No. ARG37407

ACTC1 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

This CRISPR/Cas9-edited polyclonal ACTC1 knockout HeLa cell population offers a heterogeneous loss-of-function model for studying cardiac alpha-actin function in the widely used cervical adenocarcinoma HeLa line. The pooled format avoids clonal artifacts and enables analysis of gene disruption effects across diverse edited alleles. ACTC1 encodes a sarcomeric actin that interacts with tropomyosin and is transcriptionally governed by SRF and GATA4. In HeLa cells, its knockout perturbs actin filament organization and may induce compensatory actin isoform expression. The model is suited for cytoskeletal dynamics studies, cancer-relevant migration assays, and drug screening targeting actin regulators.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    ACTC1

    Gene Identifier

    NCBI Gene ID 70

    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 ACTC1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the ACTC1 gene in HeLa cells. This heterogeneous pool offers a robust loss-of-function model free from clonal selection artifacts, suitable for pooled functional studies of cardiac alpha-actin disruption in a human epithelial context.

HeLa cells are an immortalized human cervical adenocarcinoma epithelial line, extensively utilized in cancer biology, cell signaling, and drug discovery. Their rapid proliferation, high transfection efficiency, and well-characterized genomic landscape make them an ideal host for CRISPR-mediated gene editing and reproducible downstream assays.

ACTC1 encodes alpha-cardiac actin, a core component of sarcomeric thin filaments in cardiac muscle, where it interacts with tropomyosin, the troponin complex, alpha-actinin, cofilin, and profilin to mediate actin filament dynamics and stability. Its transcription is activated by cardiogenic transcription factors including SRF, GATA4, NKX2-5, and MEF2C, downstream of TGF-beta, mechanical stress, and calcium signaling. ACTC1 is integral to sarcomere assembly and links to intercalated disc components such as N-cadherin and connexins, as well as myofibrillar proteins like myosin heavy chain. In the HeLa context, ACTC1 knockout is predicted to alter actin polymerization and cytoskeletal mechanics, potentially inducing compensatory upregulation of other actin isoforms like ACTB and ACTG1.

In this non-muscle epithelial background, ACTC1 knockout provides a unique model to dissect isoform-specific actin functions without the confounding presence of sarcomeric structures. The polyclonal pool allows for the evaluation of heterogeneous gene disruption effects on cellular processes such as adhesion, migration, and proliferation, which are critical in cancer progression. It also facilitates study of how cancer cells compensate for loss of a minor actin isoform, shedding light on cytoskeletal plasticity.

This knockout model is applicable to a variety of functional assays, including immunofluorescence microscopy for actin cytoskeleton visualization, wound healing and migration assays, co-immunoprecipitation of interacting partners, and RNA-seq transcriptome analysis to map gene expression changes. It is suitable for studying compensatory actin isoform responses and for screening small molecules that target actin dynamics. For additional product details, please contact Ascent Research.

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