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Cat. No. ARG33866

APMAP Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

The APMAP Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human Jurkat T lymphocyte line. This model provides a loss-of-function tool to investigate APMAP, a transmembrane protein linked to adipocyte function, insulin sensitivity, and extracellular matrix organization. APMAP is regulated by PPARG and insulin and influences downstream targets such as GLUT4 and lipid droplet proteins through interactions with integrins and ECM components. These cells are suited for studying APMAP's non-adipocyte roles in T-cell biology, cell adhesion, and metabolic signaling, with applications in obesity and type 2 diabetes research and drug screening.

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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

    APMAP

    Gene Identifier

    NCBI Gene ID 57136

    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 APMAP Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human Jurkat T lymphocyte line. This product provides a targeted disruption of the APMAP gene, resulting in a loss-of-function model that eliminates APMAP expression in a heterogeneous cell pool. The polyclonal format preserves the natural diversity of gene-editing outcomes, making it well suited for population-level functional studies without the constraints of clonal selection. These cells are supplied as a ready-to-use resource for advanced research applications.

Jurkat cells are an immortalized T-cell leukemia line widely used in immunology to study T-cell receptor signaling, apoptosis, and cytokine production. Their well-characterized pathways and robust growth make them ideal for CRISPR knockout studies. This background allows isolation of APMAP-specific functions in non-adipocyte contexts, such as T-cell adhesion and signaling.

APMAP encodes a transmembrane protein involved in adipocyte biology, where it integrates signals from PPARG and insulin to modulate adipogenesis, insulin sensitivity, and extracellular matrix (ECM) organization. Mechanistically, APMAP acts at the nexus of ECM and metabolic signaling: it interacts with ECM proteins and integrins, and influences downstream targets such as glucose transporter GLUT4, insulin receptor substrates, and lipid droplet proteins. Within the adipogenic cascade, APMAP is associated with transcription factors CEBPA and downstream effectors including FABP4 and ADIPOQ. This network positions APMAP as a key modulator of metabolic homeostasis linking structural cues to intracellular energy sensing.

In the Jurkat T-cell context, APMAP knockout offers a unique opportunity to delineate non-adipocyte roles of this protein. T lymphocytes do not execute endogenous adipogenic programs, so this model can reveal unexpected APMAP functions in cell adhesion, migration, or immune signaling that may be relevant to metabolic disease-associated immune dysregulation. The polyclonal knockout format enables population-level analyses, allowing assessment of heterogeneous cellular responses. This configuration is particularly useful for pathway-level studies where bulk measurements such as Western blotting, flow cytometry, or metabolic assays are employed, and it provides a complementary platform to adipocyte-focused research.

Applications include studying APMAP function in T-cell biology, investigating adipocyte pathways in a non-adipocyte setting, and drug screening for obesity and type 2 diabetes. Compatible assays are RT-qPCR, Western blotting, flow cytometry, cell adhesion, migration, and metabolic assays, enabling thorough characterization. For more information, contact Ascent Research.

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