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Cat. No. ARG35009

ARG1 Knockout 143B Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Osteosarcoma

The ARG1 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population disrupting ARG1 in 143B human osteosarcoma cells. ARG1 hydrolyzes arginine to ornithine and urea, competing with nitric oxide synthase and suppressing T-cell immunity via arginine depletion. Ornithine fuels polyamine and proline synthesis through ornithine decarboxylase, promoting tumor growth. This model supports studies of arginine metabolism, immune evasion in osteosarcoma, and arginase inhibitor screening with applications in T-cell co-culture, polyamine profiling, and xenograft models.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    143B

    Age

    13 years

    Gene Name

    ARG1

    Gene Identifier

    NCBI Gene ID 383

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM/F12

    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 ARG1 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 143B human osteosarcoma cell line, designed to disrupt the ARG1 gene encoding arginase-1. This polyclonal model provides a heterogeneous pool of genetically edited cells without clonal selection, enabling functional studies of ARG1 loss while preserving the biological variability inherent to the parental 143B line.

The parental 143B cell line is a highly tumorigenic and metastatic subline of HOS, established from a human osteosarcoma. As a malignant bone-forming cell line, 143B is extensively utilized in cancer research for its aggressive growth characteristics and robust metastatic capacity in xenograft models. Its well-characterized behavior makes it an ideal host for generating knockout models to investigate oncogenic mechanisms and tumor?Chost interactions.

Arginase-1 (ARG1) catalyzes the hydrolysis of L-arginine to L-ornithine and urea, a key reaction in the urea cycle. In the tumor microenvironment, ARG1 competes with nitric oxide synthase (NOS) for arginine, modulating nitric oxide production. ARG1 expression is regulated by IL-4 and IL-13 via STAT6, and also by TGF-??, C/EBP??, and cAMP. The resulting ornithine feeds into polyamine biosynthesis through ornithine decarboxylase (ODC) and spermidine synthase, and into proline synthesis, promoting proliferation. Importantly, ARG1-mediated arginine depletion suppresses T-cell receptor signaling, impairing T-cell function and enabling immune evasion??a mechanism relevant to osteosarcoma.

In 143B osteosarcoma cells, ARG1-driven arginine depletion may facilitate immune escape by blunting T-cell responses, while diversion into polyamines and proline supports tumor growth and metastasis. Knockout of ARG1 in this aggressive model allows dissection of its metabolic and immunomodulatory roles. The polyclonal knockout population enables assessment of collective functional impacts on proliferation, migration, and tumor?Cimmune interactions, both in vitro and in vivo.

This model is suited for applications including arginine metabolism studies, tumor immune evasion research, osteosarcoma progression analysis, and arginase inhibitor screening. Representative assays include arginase activity assays, urea/ornithine quantification, polyamine profiling, T-cell suppression co-culture, cell proliferation/migration assays, western blotting, RT-qPCR, and xenograft tumor models. For further information or technical support, contact Ascent Research.

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