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Cat. No. ARG33522

KHNYN Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

KHNYN Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell pool designed to disrupt the KHNYN gene in a human colorectal adenocarcinoma model. KHNYN is an interferon-stimulated antiviral factor that degrades viral RNA through its endonuclease domain, acting downstream of RIG-I/MAVS signaling and interacting with G3BP1 in stress granules. The HT29 background provides an intestinal epithelial context for studying innate immune responses. These cells are ideal for viral replication assays, RNA degradation studies, and stress granule analyses using western blotting, immunofluorescence, and co-immunoprecipitation. Contact Ascent Research for more information.

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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

    KHNYN

    Gene Identifier

    NCBI Gene ID 23351

    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

KHNYN Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population that enables functional studies of KHNYN in a human colorectal adenocarcinoma background. This polyclonal format ensures a heterogeneous pool of cells with targeted disruptions in the KHNYN gene, facilitating loss-of-function analyses without clonal selection bias. The CRISPR/Cas9-mediated gene disruption creates a reliable model for investigating KHNYN-dependent antiviral and RNA regulatory mechanisms.

The HT29 host cell line originates from a 44-year-old female with colorectal adenocarcinoma and is a well-characterized model of intestinal epithelial cells. These cells can differentiate into enterocyte-like cells, mimicking key aspects of the intestinal epithelium. HT29 cells are extensively used to study epithelial barrier function, mucosal immunity, and host-pathogen interactions, making them an ideal platform for examining innate immune factors such as KHNYN at mucosal surfaces.

KHNYN is an interferon-inducible RNA-binding protein with endonuclease activity, acting as a restriction factor against retroviruses like HIV-1. It binds viral RNA via its KH domain and promotes degradation through its NYN endonuclease domain. Expression is induced by type I interferons (IFN-??/??) through STAT1 and IRF9. KHNYN interacts with HIV-1 capsid and colocalizes with stress granule proteins G3BP1 and TIA1, facilitating viral RNA decay. This protein functions downstream of the RIG-I/MAVS/IRF3 antiviral signaling axis and associates with CNBP, suggesting broader roles in RNA metabolism.

In the context of HT29 cells, KHNYN knockout provides a unique model to dissect cell-intrinsic antiviral defenses in intestinal epithelia. As a primary entry site for viruses, the gut mucosa relies on interferon-induced restriction factors to limit infection. Disrupting KHNYN in these cells allows researchers to evaluate its impact on viral replication, stress granule dynamics, and innate signaling pathways, linking epithelial biology with antiviral immunity.

Applications include studying antiviral innate immunity, HIV restriction, RNA degradation, and stress granule biology. Representative assays include western blotting, RT-qPCR, RNA-seq, co-immunoprecipitation, viral replication assays, immunofluorescence, and flow cytometry. These cells support mechanistic studies of interferon-stimulated gene function and viral-host interactions. For further details, please contact Ascent Research.

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