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Cat. No. ARG36756

KLRB1 Knockout SKOV3 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

KLRB1 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of the human ovarian adenocarcinoma cell line SK-OV-3, in which the gene encoding the C-type lectin receptor CD161 has been functionally disrupted. This knockout model enables loss-of-function investigation of the CD161?CCLEC2D (LLT1) signaling axis, which modulates immune cell cytotoxicity and cytokine production through downstream effectors such as PTPN6, PTPN11, SYK, and AKT1. Applications include co-culture assays with NK cells to study tumor-immune interactions, cytokine profiling by ELISA, and signaling pathway analysis using western blotting and RT-qPCR. These polyclonal cells provide a versatile platform for elucidating CD161-mediated regulatory mechanisms in ovarian cancer and autoimmune disease research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    SKOV3

    Sex of Donor

    Female

    Age

    64 years

    Derived From Site

    Ascites

    Gene Name

    KLRB1

    Gene Identifier

    NCBI Gene ID 3820

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 KLRB1 Knockout SK-OV-3 Polyclonal Cells product provides a polyclonal population of SK-OV-3 cells in which the KLRB1 gene has been disrupted via CRISPR/Cas9-mediated genome editing. These polyclonal knockout cells enable loss-of-function studies of the KLRB1-encoded CD161 receptor within a heterogeneous cell pool, reflecting a more natural mixture of edited genotypes compared to monoclonal lines. This format is well suited for examining bulk cellular responses and population-level phenotypes in immune receptor research.

The host cell line, SK-OV-3, is a well-established human ovarian adenocarcinoma epithelial line originally derived from the ascites of a patient with ovarian cancer. SK-OV-3 cells are widely employed as a model system for studying ovarian cancer biology, including tumor cell signaling, drug resistance, and interactions with immune components. Their epithelial origin and molecular characteristics make them a relevant platform for investigating tumor-immune crosstalk in an adenocarcinoma context.

KLRB1 encodes CD161, a C-type lectin receptor expressed on natural killer (NK) and T cell subsets. Upon binding its ligand CLEC2D (LLT1), CD161 transmits inhibitory or activating signals that modulate immune cell cytotoxicity and cytokine production. CD161 signaling is regulated by upstream factors including interleukin-12 (IL-12), IL-15, and the transcription factors RORC and TBX21. Downstream, CD161 engagement influences the activity of the phosphatases PTPN6 and PTPN11, the kinase SYK, and AKT1, ultimately affecting interferon-gamma (IFNG) expression. This pathway integrates extracellular cues to govern immune cell effector functions within the tumor microenvironment.

In the context of ovarian cancer, CD161?CLLT1 interactions may contribute to immune evasion or modulation of anti-tumor responses. Dysregulation of this axis has been implicated in cancer and autoimmune diseases. The use of KLRB1-disrupted SK-OV-3 cells allows investigators to dissect the role of tumor cell-expressed CD161??if present??or to employ these cells in co-culture systems where CD161 on immune effector cells can be interrogated. This model provides a valuable tool for exploring how CD161 signaling influences ovarian cancer cell behavior and immune cell crosstalk.

These polyclonal knockout cells are suitable for a range of experimental applications, including functional assays examining tumor-immune interactions, co-culture models with NK cells to assess cytotoxicity, and signaling studies of the CD161/LLT1 axis. Researchers can validate target disruption via western blotting and RT-qPCR, confirm CD161 loss by flow cytometry, and measure cytokine secretion using ELISA. Apoptosis assays can further delineate the impact of KLRB1 disruption on cell death pathways. For further details or to inquire about product availability, please contact Ascent Research.

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