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Cat. No. ARG38725

ANGEL1 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The ALDH9A1 Knockout A-549 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of ALDH9A1 in A-549 human lung adenocarcinoma cells. ALDH9A1 encodes an NAD+-dependent aldehyde dehydrogenase that converts gamma-aminobutyraldehyde to GABA and betaine aldehyde to betaine, regulated by NFE2L2 and SP1. This loss-of-function model enables study of GABA biosynthesis, aldehyde detoxification, and betaine metabolism in a lung epithelial cancer context. Applications include functional genomics, cancer metabolism assays, and drug resistance screens. Representative techniques such as ALDH activity assays, GABA quantification, and proliferation/apoptosis assays facilitate investigation of ALDH9A1-dependent pathways. For further details, contact Ascent Research.

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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

    ANGEL1

    Gene Identifier

    NCBI Gene ID 23357

    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 ALDH9A1 Knockout A-549 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the ALDH9A1 gene in the A-549 human lung adenocarcinoma cell line. This polyclonal pool offers a heterogeneous loss-of-function model, enabling functional studies of ALDH9A1 in a cancer cell context without clonal selection artifacts.

The A-549 cell line, isolated from a 58-year-old male, is an adherent epithelial line widely used as a model of human alveolar Type II epithelium. Derived from lung adenocarcinoma, these cells retain key features of pulmonary epithelial biology, including surfactant production and responses to oxidative stress. The A-549 line is extensively employed in cancer biology, drug resistance research, and studies of lung epithelial cell function.

ALDH9A1 encodes an aldehyde dehydrogenase that catalyzes the NAD+-dependent oxidation of gamma-aminobutyraldehyde to GABA and betaine aldehyde to betaine. This enzyme thus bridges neurotransmitter metabolism and osmoregulation. ALDH9A1 is transcriptionally regulated by NFE2L2 (Nrf2) and SP1 and is responsive to oxidative stress and PPAR??. In GABA biosynthesis, ALDH9A1 functions downstream of GAD1 and ABAT, and it interacts with NAD+, ABAT, ALDH5A1, and GAD1. Its product GABA acts on GABA receptors (GABRA1, GABRB2), while betaine supports BHMT-mediated methyl donation. Disruption of ALDH9A1 can impair aldehyde detoxification and alter signaling pathways affecting cell proliferation and apoptosis.

In A-549 lung adenocarcinoma cells, ALDH9A1 knockout may compromise GABA synthesis and betaine production, potentially influencing cell growth, migration, and stress responses. Given the role of aldehydes in oxidative damage and the known involvement of aldehyde dehydrogenases in cancer drug resistance, this model allows investigation of how loss of ALDH9A1 affects tumor cell behavior. The polyclonal knockout population is particularly useful for studying heterogeneous responses to aldehydic stress and for screening modulators of the ALDH9A1 pathway.

This polyclonal knockout cell product is suited for functional genomics, cancer metabolism studies, and investigation of neurotransmitter metabolism in non-neuronal cells. Representative assays include ALDH enzyme activity measurement, GABA quantification by ELISA or LC-MS, cell proliferation (MTS/MTT), apoptosis (Annexin V), migration (scratch wound), and drug sensitivity screens. Researchers can use these cells to explore roles of ALDH9A1 in aldehyde detoxification, drug resistance mechanisms, and tumor microenvironment interactions. For further technical information or inquiries, please contact Ascent Research.

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