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Cat. No. ARG36479

BTN1A1 Knockout NCI-H1299 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Carcinoma

The BTN1A1 Knockout NCI-H1299 Polyclonal Cells offer a CRISPR/Cas9-edited polyclonal population from the NCI-H1299 lung adenocarcinoma line with targeted disruption of the BTN1A1 immune checkpoint gene. BTN1A1 negatively regulates T cell activation by interacting with the TCR complex and attenuating ZAP70-dependent signaling, leading to reduced IL-2 production and T cell anergy. This model is particularly suited for studying immune evasion in non-small cell lung cancer, as BTN1A1 knockout is expected to relieve T cell suppression. Key applications include co-culture assays, flow cytometric measurement of activation markers (CD69, CD25), ELISA for cytokines, and validation of immunotherapeutic targets.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    NCI-H1299

    Sex of Donor

    Male

    Age

    43 years

    Gene Name

    Btn1a1

    Gene Identifier

    NCBI Gene ID 696

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    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

This product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human NCI-H1299 lung adenocarcinoma cell line, featuring targeted disruption of the BTN1A1 gene. The polyclonal format yields a heterogeneous mixture of cells with gene disruption, minimizing clonal variability and facilitating robust functional analyses. Cells are supplied as a live, adherent culture ready for use in immunological and cancer biology studies.

The NCI-H1299 cell line was derived from the lymph node metastasis of a lung adenocarcinoma from a 43-year-old Caucasian male, and it is a well-established model for non-small cell lung cancer (NSCLC) metastasis. This epithelial line retains key metastatic properties and is commonly used to investigate tumor-immune interactions and the molecular mechanisms underlying lung cancer progression.

BTN1A1 is an immune checkpoint molecule that suppresses T cell activation by interacting with an as-yet-unidentified T cell receptor, leading to reduced TCR signaling. It associates with TCR complex components such as CD3 and ZAP70, and recruits SHP-1/SHP-2 phosphatases to attenuate proximal signaling, diminishing LAT and NF-??B activation and ultimately reducing IL-2 production and promoting T cell anergy. BTN1A1 expression is regulated by IFN-??, TNF-??, and NF-??B, and it cooperates with other butyrophilin family members like BTN3A1 to modulate immune responses.

In the context of NCI-H1299 lung cancer cells, BTN1A1 knockout is anticipated to relieve immune suppression, potentially restoring T cell effector functions and enhancing anti-tumor immunity. This model allows dissection of tumor-intrinsic immunomodulatory roles of BTN1A1, and it may reveal how disruption of BTN1A1 alters NF-??B signaling and cytokine expression profiles within cancer cells, influencing the tumor microenvironment and metastatic behavior.

These polyclonal knockout cells are suited for a variety of research applications, including co-culture assays with T cells to assess activation markers (CD69, CD25) by flow cytometry, quantification of IL-2 and IFN-?? secretion by ELISA, and phospho-signaling analysis of ZAP70 and LAT. Additional uses include migration, invasion, and apoptosis assays, Western blotting, and RT-qPCR for downstream targets. This model supports immune checkpoint functional studies, cancer immunotherapy target validation, and investigation of autoimmune disease mechanisms. For further technical details or to request customization, please contact Ascent Research.

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