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Cat. No. ARG27676

KHNYN Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

KHNYN Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the near-haploid HAP1 cell line, providing a loss-of-function model for the antiviral cofactor KHNYN. KHNYN cooperates with ZAP to recognize and degrade CpG-rich viral RNA via the RNA exosome complex, linking interferon signaling to viral restriction. These cells are ideal for studies of innate antiviral immunity, interferon-stimulated gene function, and RNA decay pathways, with applications in HIV-1 infectivity assays, co-immunoprecipitation, RT-qPCR, and RNA-seq. The HAP1 background simplifies genetic screens and viral host factor discovery.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    KHNYN

    Gene Identifier

    NCBI Gene ID 23351

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    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 HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population providing a loss-of-function model for the KHNYN gene. Derived from the HAP1 cell line, these cells enable studies of KHNYN-dependent functions without specific editing details, offering a heterogeneous disruption of the target gene suitable for antiviral immunity and RNA metabolism research in a near-haploid background.

The HAP1 cell line is a near-haploid human line from a male chronic myeloid leukemia patient, harboring the Philadelphia chromosome (BCR-ABL1 translocation) and disomy for chromosome 8. Its near-haploid karyotype simplifies genetic manipulation, requiring disruption of only a single allele for many genes, making it ideal for functional genomics and viral host factor screens.

KHNYN acts as a cofactor for the antiviral zinc finger protein ZAP (ZC3HAV1), binding CpG-rich viral RNA and recruiting the RNA exosome complex (EXOSC10, DIS3) to degrade target RNA, thereby inhibiting viral replication. It is upregulated by type I interferons via IRF3/IRF7 downstream of RIG-I/MDA5/MAVS, and interacts with TRIM25 and XRN1. KHNYN thus bridges innate immune signaling and RNA decay to restrict retroviruses like HIV-1 and other RNA viruses.

In HAP1 cells, KHNYN knockout eliminates the need to consider allelic redundancy, providing a clean loss-of-function model for dissecting the ZAP-KHNYN antiviral axis. This system is valuable for studying restriction of CpG-rich viruses, retrotransposon control, and interferon-stimulated responses. Because HAP1 retains intact interferon signaling, the knockout allows assessment of how KHNYN contributes to the antiviral state induced by type I IFNs.

Applications include western blotting and genomic PCR for knockout validation, co-immunoprecipitation for ZAP or exosome interactions, RT-qPCR and RNA-seq for gene expression profiling, and HIV-1 infectivity luciferase assays to measure viral replication. The cells support interferon stimulation experiments, flow cytometry for viral antigens, and RNA immunoprecipitation. For further information and ordering, contact Ascent Research.

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