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Cat. No. ARG33863

API5 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

API5 Knockout Jurkat Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population of human Jurkat T lymphocytes, targeting the anti-apoptotic factor API5. API5 inhibits caspase-9 activation and interacts with Acinus to block apoptosis, and its expression is driven by FGF-2/EGF signaling. This model is ideal for studying apoptosis regulation, chemoresistance, and survival signaling in a leukemic background. Applications include Western blotting, flow cytometry (Annexin V), drug sensitivity assays, and co-immunoprecipitation to investigate API5-mediated pathways. The Jurkat cell line serves as a relevant model for T-cell leukemia and apoptosis research, enabling dissection of FGF signaling and caspase cascades.

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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

    API5

    Gene Identifier

    NCBI Gene ID 8539

    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 API5 Knockout Jurkat Polyclonal Cells are a human T-lymphocyte population engineered via CRISPR/Cas9 to disrupt the endogenous API5 gene. This polyclonal knockout product comprises a heterogeneous pool of edited cells, enabling studies of API5 loss without clonal selection bias. It is designed for advanced research into apoptosis, chemoresistance, and T-cell signaling.

Jurkat cells are an immortalized human T-cell leukemia line derived from an acute lymphoblastic leukemia patient. They serve as a classic model for T-cell receptor signaling, activation-induced cell death, and leukemic transformation, providing a physiologically relevant backdrop for interrogating anti-apoptotic mechanisms.

API5 (Apoptosis Inhibitor 5) suppresses apoptosis by directly binding caspase-9 to prevent its activation and by interacting with Acinus to block DNA fragmentation. Upstream, API5 expression is induced by FGF-2 and EGF via FGFR/EGFR, ERK1/2, and E2F transcriptional activation. API5 also interacts with PRPF19, a spliceosomal component, potentially linking survival signaling to mRNA processing. This positions API5 as a key node in the apoptosis-inhibitory network, frequently exploited by cancer cells for chemoresistance.

In Jurkat T-cell leukemia, API5 helps sustain malignant survival by antagonizing both intrinsic and extrinsic apoptotic signals. CRISPR/Cas9-mediated disruption of API5 in this polyclonal population allows assessment of altered caspase cascades, apoptotic thresholds, and drug sensitivity. The model is valuable for dissecting FGF-2/PI3K/AKT-mediated survival and investigating chemoresistance mechanisms in T-cell malignancies.

These cells are suitable for Western blotting to assess caspase-9 cleavage, flow cytometry for Annexin V staining, drug sensitivity assays, co-immunoprecipitation of API5 complexes, and RNA-seq for transcriptomic changes. The polyclonal format supports population-level analyses and screening applications. For additional technical details or custom inquiries, please contact Ascent Research.

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