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Cat. No. ARG43378

CD14 Knockout 769-P Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

  • Disease:

    Renal cell carcinoma

The CD14 Knockout 769-P Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CD14 gene in the human 769-P clear cell renal carcinoma line. CD14 is a co-receptor for LPS that activates TLR4/MyD88-dependent NF-kB and MAPK pathways, driving expression of pro-inflammatory cytokines such as TNF, IL-6, and IL-1??. This knockout model facilitates investigations into innate immune signaling in renal cancer, TLR4-mediated inflammation, and CD14-dependent gene regulation. It supports assays including Western blotting, NF-kB reporter, ELISA, and cytokine profiling, suitable for research in immunology, oncology, and therapeutic discovery.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    769-P

    Sex of Donor

    Female

    Age

    63 years

    Derived From Site

    In situ; Kidney

    Gene Name

    CD14

    Gene Identifier

    NCBI Gene ID 929

    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

The CD14 Knockout 769-P Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting CD14 in the human 769-P renal cell carcinoma line. This product comprises a heterogeneous pool of cells with CRISPR/Cas9-mediated gene disruption, providing a loss-of-function model for studying CD14 functions in innate immunity and cancer. The polyclonal format enables population-level analyses without clonal bias, suitable for signaling and cytokine assays.

The 769-P cell line is a model of clear cell renal cell carcinoma (ccRCC), derived from a primary tumor of a 63-year-old female. It retains characteristic ccRCC features, including dysregulated hypoxia signaling, making it a relevant system for investigating tumor-intrinsic immune signaling. The CD14 knockout in this background allows dissection of innate immune contributions to renal carcinoma biology.

CD14 serves as a co-receptor for bacterial lipopolysaccharide (LPS). It binds LPS and transfers it to the TLR4/MD-2 complex, initiating MyD88-dependent signaling that activates NF-kB and MAPK pathways. Key upstream regulators include LPS-binding protein (LBP), IL-1??, and TNF. The TLR4 complex engages IRAKs and TRAF6, leading to activation of NF-kB and MAPKs (ERK, JNK, p38), which drive transcription of pro-inflammatory cytokines such as TNF, IL-6, and IL-1??. CD14 is thus a critical node in TLR4-mediated innate immune responses and cytokine production.

In ccRCC, CD14-mediated signaling may modulate the tumor inflammatory microenvironment. This knockout model enables study of how CD14 loss impacts LPS-induced NF-kB and MAPK activation, cytokine secretion, and inflammatory gene expression in renal carcinoma. Researchers can dissect CD14-dependent pathways and evaluate crosstalk between innate immunity and oncogenic processes, potentially identifying therapeutic targets for inflammation-driven cancer progression.

Applications include examining LPS-induced signaling in renal cancer, studying innate immune crosstalk in tumors, validating CD14 as a target for sepsis and sterile inflammation, and investigating inflammatory gene regulation. Representative assays are Western blotting for signaling phosphoproteins, NF-kB luciferase reporter assay, ELISA and multiplex profiling for cytokines (TNF, IL-6, IL-1??), RT-qPCR, immunofluorescence, and flow cytometry. This polyclonal knockout population is a valuable tool for immunology, cancer, and drug discovery research. For further details or ordering, please contact Ascent Research.

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