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Cat. No. ARG33797

ALDH3A2 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

CRISPR/Cas9-edited polyclonal knockout cells for ALDH3A2 in a Jurkat T-lymphocyte background. This model disrupts the gene encoding fatty aldehyde dehydrogenase, a key enzyme in long-chain aldehyde detoxification and sphingolipid metabolism, whose expression is regulated by NRF2 and PPARs. Loss of function leads to accumulation of toxic aldehydes, providing a relevant system for studying Sj?gren-Larsson syndrome and oxidative stress responses. Ideal for investigating aldehyde toxicity, lipid-mediated signaling, and therapeutic interventions in an immune cell context. Compatible with aldehyde dehydrogenase activity assays, lipidomics, and viability assessments under oxidative challenge, this polyclonal population offers a practical tool for functional genomics and drug discovery applications.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Jurkat

    Cell Type

    T cell line

    Sex of Donor

    Male

    Age

    14 years

    Derived From Site

    In situ; Peripheral blood

    Gene Name

    ALDH3A2

    Gene Identifier

    NCBI Gene ID 224

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 ALDH3A2 Knockout Jurkat Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from Jurkat human T lymphocytes, in which the ALDH3A2 gene is disrupted. This loss-of-function model enables study of fatty aldehyde dehydrogenase deficiency in a readily expandable format suitable for pooled assays, avoiding the need for clonal isolation.

Jurkat cells are an immortalized human T-cell line originally isolated from the peripheral blood of a 14-year-old male with acute T-cell leukemia. They are extensively used for probing T-cell activation, signal transduction, and immune function, owing to their well-characterized signaling networks and amenability to genetic manipulation.

The ALDH3A2 gene product is an NAD+-dependent fatty aldehyde dehydrogenase that oxidizes long-chain aliphatic aldehydes derived from fatty alcohol metabolism and sphingolipid degradation, converting them to non-toxic fatty acids. The enzyme forms a functional homodimer and is transcriptionally controlled by NRF2 under oxidative stress, with further regulation by PPAR?? and PPAR??, placing it at the intersection of aldehyde detoxification and lipid metabolism. It acts downstream of sphingosine-1-phosphate breakdown, and its loss leads to accumulation of reactive aldehydes that promote cellular damage.

In Jurkat T cells, ALDH3A2 knockout models the consequences of impaired aldehyde clearance within a lymphocyte environment. T cells depend on lipid signaling for activation and survival, so disrupted aldehyde metabolism may alter immune responsiveness and stress tolerance. This model is particularly pertinent to Sj?gren-Larsson syndrome, a rare disorder caused by ALDH3A2 mutations, enabling investigation of how aldehyde toxicity influences T-cell physiology.

Applications include mechanistic studies of fatty aldehyde dehydrogenase deficiency, high-throughput screening for compounds that mitigate aldehyde toxicity, and examination of oxidative stress responses in immune cells. The polyclonal knockout cells are compatible with aldehyde dehydrogenase activity assays, mass spectrometry-based lipidomics, reactive aldehyde quantification, RT-qPCR, western blotting, and cell viability tests under oxidative challenge. For detailed product information and technical support, please contact Ascent Research.

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