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Cat. No. ARG33848

ANXA4 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 ANXA4 knockout Jurkat polyclonal cells provide a loss-of-function model in human T lymphocytes for studying calcium-dependent phospholipid binding, NF-??B signaling, and apoptosis. ANXA4 disruption impairs membrane repair and alters the activity of NF-??B pathway components such as RELA and IKBKB. Ideal for T cell signaling research, drug screening, and cancer biology, these cells support assays including western blotting, flow cytometry, and calcium flux measurements to probe annexin-mediated processes and therapeutic targets.

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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

    ANXA4

    Gene Identifier

    NCBI Gene ID 307

    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 ANXA4 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted gene disruption of ANXA4. This model provides a genetically heterogeneous loss-of-function system in Jurkat T lymphocytes for studying annexin A4 biology without clonal selection.

Jurkat cells, derived from a patient with acute T cell leukemia, are a widely used T lymphocyte model for T cell activation, signaling, and apoptosis. Their established signaling pathways and ease of genetic manipulation make them suitable for investigating immune cell function and leukemogenesis.

Annexin A4 is a calcium-dependent phospholipid-binding protein that regulates membrane repair, exocytosis, apoptosis, and ion channel function. In response to elevated intracellular calcium, ANXA4 translocates to membranes and interacts with phospholipids, S100 proteins (such as S100A6), actin, and other annexins like ANXA2. These interactions facilitate membrane resealing and modulate downstream signaling. ANXA4 is also linked to NF-??B pathway activation: it can influence the phosphorylation and activation of IKBKB, leading to nuclear translocation of NF-??B transcription factors RELA and NFKB1, which drive expression of anti-apoptotic and pro-survival genes. Additionally, ANXA4 participates in calcium flux regulation and affects the expression of cell adhesion molecules, integrating diverse cellular signals.

In Jurkat T cells, ANXA4 knockout disrupts calcium-dependent membrane repair and impairs NF-??B signaling, resulting in altered T cell activation, increased apoptosis, and decreased survival under stress conditions. This phenotype mirrors key aspects of T cell leukemia pathogenesis and provides a platform to investigate the role of ANXA4 in other malignancies such as colorectal, breast, and gastric cancers, where ANXA4 has been associated with tumor progression and epithelial-mesenchymal transition. By uncoupling calcium homeostasis from transcriptional responses, this model enables dissection of the signaling crosstalk that sustains lymphocyte viability.

These polyclonal knockout cells are ideal for T cell signaling, apoptosis, drug screening, and cancer biology studies. Representative assays include western blotting for ANXA4 and NF-??B targets, flow cytometry for activation and apoptosis markers, RT-qPCR for NF-??B targets, calcium flux measurements, NF-??B reporter assays, co-immunoprecipitation of ANXA4 interactors, and migration/invasion assays. For further technical specifications or to discuss how this model can support your research, please contact Ascent Research.

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