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Cat. No. ARG43476

CD300C Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

This CRISPR/Cas9-edited polyclonal knockout cell population disrupts the CD300C gene in the near-haploid HAP1 cell line. CD300C is a myeloid activating receptor that couples to the DAP12 adaptor and SYK kinase, triggering NF-??B-dependent cytokine production and phagocytosis. The knockout pool provides a clean loss-of-function model for studying ITAM-mediated innate immune signaling. Researchers can use this tool for functional characterization, drug target validation in inflammatory diseases, and screening of immuno-oncology candidates. Robust applications include flow cytometry, multiplex cytokine profiling, phospho-SYK detection, and NF-??B luciferase assays. For additional information, contact Ascent Research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    CD300C

    Gene Identifier

    NCBI Gene ID 10871

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    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 CD300C Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CD300C gene in the HAP1 host. This pool contains a heterogeneous mix of gene-disrupted alleles, enabling robust functional studies without clonal artifacts. The loss-of-function model facilitates dissection of CD300C-mediated signaling in a simplified haploid genomic setting.

HAP1 is a near-haploid human male chronic myeloid leukemia (CML) cell line derived from KBM-7. Its predominantly haploid karyotype allows single-allele targeting for functional gene disruption, making it a favorite for functional genomics. The line maintains critical signaling pathways and is widely applied in CRISPR screens and cell-based assays, providing an optimal background for studying immune receptor pathways.

CD300C encodes an activating immune receptor on myeloid cells that pairs with the ITAM-containing adaptor TYROBP (DAP12). Ligand engagement, possibly phosphatidylserine, triggers DAP12 phosphorylation and recruitment of spleen tyrosine kinase SYK. This initiates a cascade involving PLC??, PKC, and the MAPK/ERK pathway, leading to NF-??B-dependent transcription of cytokines such as TNF, IL-6, and IL-10. The receptor complex also interacts with phosphatases PTPN6 (SHP-1), PTPN11 (SHP-2), and adaptors GRB2 and PLCG2, which regulate phagocytosis and cytokine output.

In HAP1 cells, CD300C disruption yields a clean system for investigating ITAM-mediated signaling, free from the confounding influence of related receptors. The haploid genotype ensures unambiguous gene?Cphenotype linkage, while the leukemic origin retains a relevant cellular context for innate immune studies. This polyclonal knockout model is particularly useful for dissecting CD300C-dependent phagocytosis and cytokine responses, offering reduced clonal bias and enhanced reproducibility in functional analyses.

Applications include functional characterization of CD300C, drug target validation for inflammatory diseases, and screening of immuno-oncology agents targeting ITAM pathways. Compatible assays range from flow cytometry and cytokine profiling to phospho-SYK Western blotting and luciferase-based NF-??B reporter assays. These tools support detailed interrogation of innate immune regulation. For more information, contact Ascent Research.

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