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Cat. No. ARG34097

IFRD1 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

This CRISPR/Cas9-edited polyclonal knockout cell population targets IFRD1 in A-549 human lung adenocarcinoma epithelial cells. IFRD1 is a transcriptional coregulator that interacts with HDAC1, HDAC2, SMARCA4, and SMARCB1 to regulate chromatin structure and gene expression upon stimulation by interferon-gamma and other cytokines, linking inflammatory and developmental signaling networks. The knockout model enables studies of lung adenocarcinoma biology, epithelial differentiation, interferon responses, and Notch pathway activity, with applications in drug screening and cystic fibrosis modifier research. This heterogeneous population avoids clonal selection bias, providing a robust system for functional genomics and pathway interrogation. Typical assays include western blotting, RT-qPCR, interferon-gamma stimulation, ChIP-qPCR, and reporter gene analysis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A549

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    Lung

    Gene Name

    IFRD1

    Gene Identifier

    NCBI Gene ID 3475

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    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 IFRD1 Knockout A-549 Polyclonal Cells provide a heterogeneous population of A-549 human lung adenocarcinoma epithelial cells with CRISPR/Cas9-mediated disruption of the IFRD1 gene. This polyclonal knockout format delivers a pooled loss-of-function model, enabling comprehensive assessment of IFRD1 ablation within an epithelial context without the bias of clonal isolation. The cells are produced via CRISPR/Cas9 gene editing to inactivate the transcriptional coregulator IFRD1.

The A-549 host cell line was isolated from the lung adenocarcinoma of a 58-year-old Caucasian male and grows as adherent epithelial-like cells. A-549 is a standard model for lung adenocarcinoma biology, epithelial barrier function, and pulmonary disease research, including studies of cystic fibrosis modifier genes and chronic obstructive pulmonary disease. These cells are widely employed for investigating epithelial responses to inflammatory cytokines.

IFRD1 functions as a transcriptional coregulator that modulates chromatin structure and gene expression by recruiting histone deacetylases HDAC1/2 and SWI/SNF components SMARCA4/SMARCB1 to target promoters. It is activated by interferon-gamma, TGFB1, and IL4, and intersects with Notch signaling through interactions with NOTCH1, RBPJ, and MAML1. Downstream, IFRD1 regulates myogenic differentiation factors MEF2C and MYOD, cytokine IL3, and chromatin remodeling complexes, positioning it at a node of inflammatory, developmental, and proliferative signaling.

In A-549 lung adenocarcinoma cells, IFRD1 knockout enables dissection of pathways critical for tumor cell differentiation, interferon responsiveness, and inflammatory regulation. This model is particularly relevant for studying Notch-driven epithelial plasticity, STAT1/JAK1/TYK2-dependent interferon signaling, and the contributions of IFRD1 to cystic fibrosis and COPD modifier networks. The heterogeneous knockout population mirrors tumor microenvironment diversity, offering advantages for drug response screening.

Key applications include interferon-gamma stimulation assays to probe STAT1 activation, RT-qPCR and western blotting for target gene and protein analysis (e.g., MEF2C, MYOD, IL3), ChIP-qPCR to assess HDAC recruitment, and Notch reporter assays. Additional uses encompass cell proliferation, migration, and invasion assays, and transcriptome-wide RNA-seq. For further product information, technical data, or assistance with experimental design, please contact Ascent Research.

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