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Cat. No. ARG42977

CCDC167 Knockout NCI-H1975 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Carcinoma

The CCDC167 Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the poorly characterized coiled-coil domain protein CCDC167 in the EGFR-mutant NCI-H1975 lung adenocarcinoma cell line. This loss-of-function model enables investigation of CCDC167??s putative roles in centrosome biology and its potential impact on cancer cell proliferation. Applications include functional genomics, centrosomal studies, cell-based assays (e.g., immunofluorescence for centrosome markers, colony formation, apoptosis), and RNA-seq to delineate downstream pathways. The product is ideal for researchers studying lung cancer biology and centrosome-related mechanisms.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    NCI-H1975

    Sex of Donor

    Female

    Gene Name

    CCDC167

    Gene Identifier

    NCBI Gene ID 154467

    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 CCDC167 Knockout NCI-H1975 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated by disruption of the CCDC167 gene in the NCI-H1975 human lung adenocarcinoma cell line. This product provides a mixed pool of edited cells carrying heterogeneous loss-of-function alleles, enabling functional studies of CCDC167 without clonal selection biases. The polyclonal format maintains genetic diversity while achieving effective gene knockout, making it suitable for pooled screening approaches or population-level phenotypic analyses.

NCI-H1975 is a well-characterized human non-small cell lung cancer (NSCLC) cell line derived from a female patient with lung adenocarcinoma. It harbors activating EGFR mutations (L858R and T790M), which confer sensitivity to first-generation EGFR tyrosine kinase inhibitors and resistance to later-generation inhibitors, respectively. This genetic background makes NCI-H1975 an extensively used model for studying EGFR-driven oncogenic signaling, drug resistance mechanisms, and the biology of lung adenocarcinoma.

CCDC167 encodes a predicted coiled-coil domain-containing protein whose precise molecular function remains uncharacterized. Coiled-coil domains typically mediate protein?Cprotein interactions, and bioinformatic analyses suggest a potential association with centrosomal structures. In currently available data, CCDC167 has no established upstream regulators, downstream targets, or interacting partners. Based on its domain architecture, it is hypothesized to participate in centrosome duplication or mitotic spindle organization, possibly contributing to cytoskeletal dynamics. The CRISPR-mediated knockout in this model will facilitate discovery of its cellular roles and interaction networks.

In the context of NCI-H1975, disruption of CCDC167 may reveal functions relevant to lung adenocarcinoma biology. Centrosome abnormalities are a hallmark of many cancers and can drive genomic instability and tumor progression. By eliminating CCDC167 expression in an EGFR-mutant NSCLC background, researchers can investigate how this gene influences centrosome integrity, cell cycle progression, and potentially the response to EGFR-targeted therapies. This model thus provides a platform to explore the intersection of centrosome biology and oncogenic signaling in a clinically relevant lung cancer context.

The CCDC167 Knockout NCI-H1975 Polyclonal Cells are designed for a range of downstream applications. Researchers can employ Western blotting to confirm loss of CCDC167 protein, immunofluorescence with centrosomal markers (e.g., ??-tubulin, pericentrin) to assess centrosome phenotypes, and colony formation, migration, or apoptosis assays to evaluate effects on cell behavior. RNA-sequencing of the knockout population can uncover transcriptomic changes and identify downstream pathways. Together, these assays support functional characterization of CCDC167 in lung cancer and centrosome biology. For additional information or technical support, please contact Ascent Research.

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