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Cat. No. ARG33025

ARHGEF10 Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The ARHGEF10 Knockout HT29 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population of human colorectal adenocarcinoma cells with disrupted ARHGEF10 expression. As a loss-of-function model in the HT29 intestinal cancer line, this product enables dissection of ARHGEF10-dependent signaling in colorectal carcinoma. ARHGEF10 encodes a Rho guanine nucleotide exchange factor that activates RhoA and RhoB, driving ROCK-mediated actin cytoskeleton reorganization and cell migration. Downstream targets include MLC and YAP/TAZ, connecting growth factor and integrin signals to motility. Ideal for wound healing, invasion, and Rho pathway-targeted drug studies.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HT29

    Gene Name

    ARHGEF10

    Gene Identifier

    NCBI Gene ID 9639

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 ARHGEF10 Knockout HT29 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of human HT29 colorectal adenocarcinoma cells with disrupted ARHGEF10 expression. This loss-of-function model avoids clonal selection artifacts and provides a heterogeneous knockout background for studying ARHGEF10-dependent signaling.

The HT29 cell line, derived from a female colorectal adenocarcinoma, maintains epithelial morphology and the capacity to differentiate into enterocyte-like cells. As a widely used intestinal cancer model, HT29 cells are instrumental for investigating colorectal carcinoma biology, including tumor cell behavior and therapeutic responses.

ARHGEF10 functions as a guanine nucleotide exchange factor for RhoA and RhoB, facilitating GDP-GTP exchange and subsequent activation. Upstream signals from EGF, TGF-??, and integrin engagement via FAK stimulate ARHGEF10, which in turn activates ROCK-dependent MLC phosphorylation and actin stress fiber formation. This pathway orchestrates cytoskeletal reorganization, focal adhesion dynamics, and cell migration. Interacting with RhoA, RhoB, F-actin, and microtubules, ARHGEF10 integrates extracellular cues with transcriptional responses mediated by YAP/TAZ and SRF/MRTF. Core pathway components include RhoA, ROCK, MLC, FAK, integrin, and paxillin.

In HT29 colorectal adenocarcinoma cells, ARHGEF10 knockout disrupts Rho GTPase signaling critical for actin dynamics and cell motility. This model allows direct assessment of how loss of ARHGEF10 affects focal adhesion turnover, migration, and invasion??processes central to colorectal cancer progression. By uncoupling upstream receptor inputs from downstream ROCK and YAP/TAZ effectors, the knockout cells serve as a defined system for studying Rho-dependent mechanisms in a disease-relevant epithelial context and for pharmacological evaluation of Rho/ROCK inhibitors.

Typical applications include wound healing and transwell invasion assays to quantify migration, immunofluorescence for F-actin organization, and RhoA GTPase activity measurements. Western blotting for ARHGEF10 and phospho-MLC confirms knockout and signaling impact, while MTT assays assess proliferation. These applications make the polyclonal knockout cells ideal for basic colorectal cancer research, drug discovery targeting Rho/ROCK pathways, and investigations of intestinal epithelial biology. For additional product or technical information, please contact Ascent Research.

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