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Cat. No. ARG35292

BMP2 Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

The BMP2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS gastric adenocarcinoma cell line, featuring targeted disruption of the BMP2 gene. BMP2 encodes a TGF-beta superfamily ligand that regulates proliferation, differentiation, and apoptosis through SMAD1/5/8-mediated transcription of targets such as ID1 and RUNX2. This loss-of-function model is designed for investigating BMP2-dependent tumor suppression mechanisms in gastric cancer, including cell proliferation, apoptosis, and signaling pathway analysis using assays like Western blot, RT-qPCR, and cell viability tests.

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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

    BMP2

    Gene Identifier

    NCBI Gene ID 650

    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 BMP2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma line, with targeted disruption of the BMP2 gene. This loss-of-function model enables investigation of BMP2, a TGF-beta superfamily ligand involved in bone formation and cell regulation, without the limitations of transient silencing. As a polyclonal population, these cells are suitable for bulk functional assays in gastric cancer research.

The AGS cell line was established from a primary gastric adenocarcinoma of a 54-year-old Caucasian female and serves as a widely used epithelial model of gastric adenocarcinoma. AGS cells retain key oncogenic features and provide a relevant background for studying tumor cell proliferation, apoptosis, and signaling. Their use in BMP2 knockout allows dissection of tumor-suppressive mechanisms within a clinically pertinent context.

BMP2 signals through heteromeric complexes of type I (BMPR1A/BMPR1B) and type II (BMPR2) receptors, leading to phosphorylation of SMAD1/5/8. These R-SMADs partner with SMAD4 to translocate to the nucleus and regulate target genes such as ID1, ID2, and RUNX2. BMP2 activity is modulated by extracellular antagonists (NOG, CHRD, GREM1) and inhibitory SMADs (SMAD6, SMAD7), and intersects with MAPK, Wnt, and PI3K-Akt pathways.

In AGS gastric cancer cells, BMP2 often acts as a tumor suppressor by inhibiting proliferation and inducing apoptosis. Mechanistically, it may upregulate p21 and downregulate BCL2 via SMAD-dependent transcription. Disruption of BMP2 in this polyclonal model enables studies of how loss of this ligand alters tumor cell behavior, including growth, survival, and metastatic potential, and how it reshapes signaling networks.

Applications include proliferation (MTT/WST-1), apoptosis (annexin V/PI flow cytometry), colony formation, and Transwell migration/invasion assays. Signaling analyses can employ phospho-SMAD1/5/8 Western blotting, RT-qPCR for ID1 and RUNX2, and immunofluorescence for SMAD localization. RNA-seq facilitates transcriptome-wide analysis of BMP2-dependent changes. These cells are also suited for drug response screening. For more information, contact Ascent Research.

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