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Cat. No. ARG37624

ARHGAP11A Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The ARHGAP11A Knockout HeLa Polyclonal Cells offer a CRISPR/Cas9-edited polyclonal knockout population in HeLa cells for loss-of-function analysis of ARHGAP11A, a RhoGAP that inactivates RhoA, Rac1, and Cdc42 to control actin dynamics and cell cycle progression. Applications include investigating Rho GTPase signaling, cytoskeletal reorganization, and proliferation in cervical cancer research, utilizing assays such as Rho activity measurements, flow cytometry, and migration studies.

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Shipping Info:

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

    ARHGAP11A

    Gene Identifier

    NCBI Gene ID 9824

    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 ARHGAP11A Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by targeted disruption of the ARHGAP11A gene in the HeLa cell line. This product delivers a heterogeneous pool of cells carrying diverse gene-editing events, providing a loss-of-function model without clonal isolation and minimizing the risk of clonal artifacts. The polyclonal format enables rapid experimental deployment for investigating ARHGAP11A biology in a cancer-relevant background.

The host HeLa cell line is an immortalized human cervical carcinoma line widely employed as a model system in cancer research. HeLa cells are characterized by robust proliferation, straightforward culture conditions, and thoroughly documented signaling pathways, making them a standard platform for studying oncogenic processes, cell cycle control, and cytoskeletal dynamics.

ARHGAP11A encodes a Rho GTPase-activating protein (RhoGAP) that stimulates GTP hydrolysis on Rho family GTPases such as RhoA, Rac1, and Cdc42, converting them to an inactive GDP-bound state. This inactivation serves as a key regulatory node in actin cytoskeleton reorganization and cell cycle progression. ARHGAP11A expression is controlled by E2F transcription factors and mitogenic signals, and its activity modulates the RhoA?CRock?CLIMK?Ccofilin axis, directly impacting actin dynamics. ARHGAP11A interacts with Rho GTPases, G-actin, and F-actin, positioning it at the intersection of growth factor signaling and cytoskeletal remodeling.

In the HeLa cervical carcinoma context, ARHGAP11A disruption may impair cytokinesis and alter proliferation, modeling the consequences of RhoGAP dysfunction in malignant cells. This knockout system enables dissection of how aberrant actin regulation contributes to division defects and the cytoskeletal abnormalities observed in cancer, offering a path to examine Rho GTPase-driven mechanisms in tumor cell biology.

This polyclonal knockout cell population is suited for a broad range of experimental applications, including cell cycle analysis by flow cytometry, Rho GTPase activity assays, western blotting, and immunofluorescence for actin architecture visualization. Functional studies such as proliferation, migration, and invasion assays can be performed to assess ARHGAP11A??s role in cancer cell behavior, and the cells are amenable to Hippo pathway investigations given the cross-talk between Rho GTPases and YAP/TAZ regulation. For further information and technical support, please contact Ascent Research.

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