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Cat. No. ARG31998

AKR7A2 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The AKR7A2 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human A-549 lung adenocarcinoma cells with targeted gene disruption of AKR7A2. This loss-of-function model enables studies of aldo-keto reductase-mediated detoxification, NRF2-dependent oxidative stress responses, and chemoresistance mechanisms in an epithelial context. AKR7A2 catalyzes NADPH-dependent reduction of reactive aldehydes such as 4-HNE, acting downstream of NRF2 and cooperating with targets like AKR1C1, NQO1, and GCLC. These cells support applications in drug sensitivity assays, 4-HNE quantification, NRF2 reporter assays, and oxidative stress modeling.

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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

    AKR7A2

    Gene Identifier

    NCBI Gene ID 8574

    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

AKR7A2 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human A-549 lung carcinoma cells harboring targeted disruption of the AKR7A2 gene. This gene-edited pool provides a heterogeneous loss-of-function model without clonal isolation, allowing investigation of aldo-keto reductase family 7 member A2 (AKR7A2) deficiency at the population level in an epithelial background.

The A-549 cell line was established from lung adenocarcinoma tissue of a 58-year-old male and displays adherent epithelial morphology. It serves as a well-characterized model of human alveolar type II epithelium and is widely used in studies of lung cancer biology, drug metabolism, and respiratory infections, making it a relevant host for probing the function of detoxification enzymes in pulmonary adenocarcinoma.

AKR7A2 is an NADPH-dependent aldo-keto reductase that reduces cytotoxic aldehydes such as 4-hydroxy-2-nonenal (4-HNE) to less reactive alcohols, thereby decreasing protein carbonylation and protecting against lipid peroxidation. Its expression is activated by NRF2 (NFE2L2) transcription factors following oxidative or electrophilic stress, functioning downstream of the KEAP1?CNRF2?CARE signaling axis. The enzyme interacts with NADPH and substrates like 4-HNE and acrolein, and acts in concert with other NRF2 targets including AKR1C1, NQO1, and GCLC to mediate cellular antioxidant defenses.

In A-549 cells, AKR7A2 contributes to the detoxification of reactive aldehydes and may influence resistance to pro-oxidant chemotherapeutics. Disruption of AKR7A2 is anticipated to impair the reduction of 4-HNE, sensitizing cells to oxidative damage and providing a system to study NRF2-driven cytoprotection and drug sensitivity in lung adenocarcinoma. This model enables dissection of how aldo-keto reductase activity modulates stress responses and chemoresistance in an epithelial context.

The knockout cells are suitable for chemoresistance screening via MTT or CellTiter-Glo viability assays, direct 4-HNE quantification, NRF2 luciferase reporter assays, RT-qPCR analysis of NRF2 target genes, and immunoblotting. They can also be used for TBARS-based lipid peroxidation measurement and ROS detection. These applications support functional characterization of AKR7A2 in lung epithelial biology and oxidative stress pathways. For further information, please contact Ascent Research.

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