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Cat. No. ARG43376

CD109 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

CD109 knockout Jurkat polyclonal cells are a CRISPR/Cas9-edited cell population derived from the Jurkat human T lymphocyte line, designed for targeted disruption of CD109. CD109, a GPI-anchored glycoprotein, negatively regulates TGF-?? signaling by interacting with TGFBR1/TGFBR2 and inhibiting SMAD2/3 phosphorylation, and its knockout enables investigation of roles in T-cell proliferation, survival, and leukemia biology. Suitable for applications such as phospho-SMAD2/3 Western blotting, SMAD luciferase reporter assays, apoptosis flow cytometry, and MTT proliferation assays, these cells are ideal for studying TGF-?? signaling in T-cell acute lymphoblastic leukemia, screening for disease regulators, and exploring CD109-dependent therapeutic vulnerabilities.

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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

    CD109

    Gene Identifier

    NCBI Gene ID 135228

    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

CD109 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte line, with targeted disruption of CD109. This heterogeneous pool contains cells carrying diverse loss-of-function mutations in CD109, offering a versatile model for studying gene function without clonal bias. The product is intended for advanced biomedical research on T-cell signaling and leukemia.

The Jurkat cell line is an immortalized T-cell model established from the peripheral blood of a 14-year-old male with acute T-cell leukemia (T-ALL). Widely used to study T-cell receptor signaling, cytokine responses, and apoptosis, Jurkat cells retain key features of T lymphoblasts and serve as a robust system for investigating the molecular basis of T-ALL.

CD109 encodes a glycosylphosphatidylinositol-anchored glycoprotein that negatively regulates transforming growth factor-?? (TGF-??) signaling by binding TGFBR1 and TGFBR2, thereby inhibiting phosphorylation of SMAD2 and SMAD3. This attenuates SMAD-dependent transcription of targets such as SERPINE1 and CDKN1A. CD109 expression is regulated by TGFB1, interleukin-13, and T-cell receptor activation, and it modulates STAT3 activity, linking to JAK/STAT and PI3K/AKT pathways. Homodimerization further influences its receptor interaction, positioning CD109 as a key modulator at the nexus of several signaling networks.

In Jurkat T cells, TGF-?? signaling controls proliferation and survival. CD109 disruption may sensitize cells to TGF-??, potentially enhancing SMAD2/3 phosphorylation, altering expression of downstream targets, and shifting cell cycle or apoptotic responses. This model is particularly valuable for exploring T-ALL pathogenesis, where TGF-?? pathway dysregulation is common, and for dissecting how CD109 contributes to leukemogenesis.

Key applications include Western blotting for CD109 and phospho-SMAD2/3, SMAD-responsive luciferase reporter assays, annexin V flow cytometry for apoptosis monitoring, and MTT proliferation assays. RT-qPCR can quantify changes in TGF-?? target genes. This product supports studies of TGF-?? signaling in leukemia, screening for T-ALL regulators, and therapeutic target discovery. For more information, please reach out to Ascent Research.

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