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Cat. No. ARG43490

CD300ld Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

CD300LD Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HeLa cervical adenocarcinoma line, enabling loss-of-function studies of the inhibitory immunoreceptor CD300LD. This receptor signals via ITIM-mediated recruitment of SHP-1 and SHP-2 phosphatases to dampen ITAM-driven activation of PI3K/AKT and NF-??B. Ideal for investigating CD300LD function in epithelial cancer models, immune checkpoint mechanisms, and tumor microenvironment signaling, these cells support assays such as Western blotting, co-immunoprecipitation, cytokine ELISA, and reporter gene analyses. Contact Ascent Research for more information.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    CD300LD

    Gene Identifier

    NCBI Gene ID 100131439

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    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 CD300LD Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line, designed for targeted disruption of the CD300LD gene. This pool of genetically heterogeneous knockout cells provides a robust loss-of-function model for studying CD300LD-mediated inhibitory signaling without the limitations of clonal variation.

The parental HeLa cell line is a well-characterized, adherent epithelial model originally isolated from a cervical carcinoma, and it harbors integrated human papillomavirus type 18 (HPV18) sequences. These immortalized cells are widely employed in cancer biology, signal transduction, and drug discovery research due to their ease of culture, genetic tractability, and established use in functional genomics.

CD300LD is an inhibitory immunoreceptor containing immunoreceptor tyrosine-based inhibitory motifs (ITIMs) that, upon engagement by unidentified endogenous ligands (possibly lipid mediators such as phosphatidylserine), undergoes phosphorylation by Src family kinases including Lyn and Fyn. This triggers recruitment and activation of SHP-1, SHP-2, and SHIP phosphatases, leading to dephosphorylation of proximal signaling molecules, attenuation of ITAM-mediated activation pathways, and suppression of downstream effectors such as PI3K/AKT and NF-??B, ultimately reducing calcium mobilization and pro-inflammatory cytokine production.

In the HeLa epithelial carcinoma context, CD300LD knockout enables dissection of the receptor??s intrinsic signaling properties and its potential contributions to tumor cell-intrinsic immune evasion or modulation of inflammatory responses. While CD300LD is predominantly studied in myeloid cells, ectopic expression or endogenous low-level expression in epithelial tumor lines can be investigated using this polyclonal knockout pool to assess impacts on cell proliferation, migration, or cytokine profiles, providing a versatile platform for immune checkpoint research.

Researchers can employ these cells in a variety of experimental workflows, including Western blotting to confirm CD300LD loss and monitor ITIM phosphorylation, flow cytometry to quantify surface receptor expression, co-immunoprecipitation to assess interactions with SHP-1 or SHP-2, and NF-??B luciferase reporter assays to evaluate downstream signaling. Additional applications include cytokine secretion profiling by ELISA for TNF-?? and IL-6, phospho-AKT analysis, and RNA sequencing to characterize global transcriptomic changes. For further details or to request a quotation, please contact Ascent Research.

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