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Cat. No. ARG43106

CCDC90B Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

The CCDC90B Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of AGS human gastric adenocarcinoma cells, designed to disrupt expression of the mitochondrial coiled-coil domain protein CCDC90B. This loss-of-function model facilitates investigation of CCDC90B??s involvement in mitochondrial homeostasis, energy metabolism, and apoptosis in gastric cancer. Knockout of CCDC90B may impair mitochondrial respiratory chain activity and modulate BCL-2 family?Cmediated apoptotic signaling. The polyclonal pool is ideally suited for functional genomics, target validation, and metabolic profiling using techniques such as Seahorse flux analysis, JC-1 staining, and Annexin V assays.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    AGS

    Sex of Donor

    Female

    Age

    54 years

    Derived From Site

    In situ; Stomach

    Gene Name

    CCDC90B

    Gene Identifier

    NCBI Gene ID 60492

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    Ham's F-12

    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 CCDC90B Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line. This pooled model introduces loss-of-function mutations in the CCDC90B gene, which encodes a mitochondrial coiled-coil domain-containing protein. The polyclonal format retains genetic heterogeneity, allowing robust assessment of gene function without clonal selection bias, and is optimized for in vitro assays probing mitochondrial roles in gastric cancer.

AGS is an epithelial cell line established from a gastric adenocarcinoma and serves as a prevalent model for studying gastric carcinogenesis. Its adherent growth and well-characterized genomic landscape facilitate gene editing and downstream phenotypic analyses. The CCDC90B knockout derivatives preserve the malignant features of the parental line, enabling direct comparison between wild-type and gene-disrupted populations to discern CCDC90B-specific contributions to tumor cell behavior.

CCDC90B localizes to mitochondria and contains a coiled-coil domain suggestive of protein?Cprotein interaction functions. Though its regulatory network remains poorly defined, CCDC90B is implicated in mitochondrial homeostasis, with mechanistic links to respiratory chain complexes, BCL-2 family members (e.g., BAX, BAK), cytochrome c release, and caspase activation. Disruption of CCDC90B is therefore predicted to impair mitochondrial integrity, potentially shifting the balance of pro- and anti-apoptotic signals and altering cellular energy metabolism.

In AGS gastric cancer cells, which often depend on robust mitochondrial activity for proliferation and survival, CCDC90B knockout provides a defined model to study metabolic vulnerability and apoptotic sensitivity. The polyclonal design mitigates clonal artifacts, ensuring that phenotypes??such as reduced metabolic flux, decreased colony formation, or enhanced apoptosis under stress??reflect authentic gene-dependent effects. This makes the model particularly valuable for target validation studies in gastric oncology.

This product supports a broad array of experimental techniques, including western blotting and RT-qPCR for expression profiling, MTT and colony formation assays for growth assessment, JC-1 and Seahorse analyses for mitochondrial membrane potential and bioenergetics, and Annexin V staining for apoptosis detection. These tools enable comprehensive dissection of CCDC90B??s role in mitochondrial function and cell death pathways. For further information, please contact Ascent Research.

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