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Cat. No. ARG34729

BMPR1A Knockout HCT116 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Large intestine (colon)

  • Disease:

    Carcinoma

BMPR1A Knockout HCT 116 Polyclonal Cells are CRISPR/Cas9-edited polyclonal knockout cells based on the HCT 116 colorectal carcinoma line, with targeted disruption of the BMPR1A gene. BMPR1A encodes the type I BMP receptor that transmits signals from BMP2/BMP4 ligands via SMAD1/5/8 to regulate ID1 and CDKN1A, functioning as a tumor suppressor in the colorectum. This model is ideal for colorectal cancer research, juvenile polyposis studies, and BMP pathway drug screening. Applications include Western blotting for phospho-SMAD1/5/8, RT-qPCR for ID1/ID2, apoptosis assays, and xenograft studies for detailed analysis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HCT 116

    Sex of Donor

    Male

    Age

    Adult

    Derived From Site

    In situ; Colon

    Gene Name

    BMPR1A

    Gene Identifier

    NCBI Gene ID 657

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 BMPR1A Knockout HCT 116 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal carcinoma cell line HCT 116, engineered to disrupt the BMPR1A gene. This targeted gene disruption generates a loss-of-function model for the BMP type IA receptor, a critical serine/threonine kinase receptor in the BMP signaling pathway. The polyclonal format provides a diverse cell population suited for robust functional studies without clonal bias.

The parental HCT 116 cell line is a widely used colorectal cancer model characterized by microsatellite instability-high (MSI-H) and oncogenic mutations in KRAS (G13D) and PIK3CA, while maintaining wild-type TP53. This genetic background mirrors key molecular features of human colorectal tumors, making it valuable for tumorigenesis research and drug testing.

BMPR1A encodes a receptor that, upon ligand binding by BMP2, BMP4, BMP6, BMP7, or GDF5, forms a complex with BMPR2 and phosphorylates SMAD1, SMAD5, and SMAD8. These activated SMADs associate with SMAD4 to regulate transcription of downstream targets, including the ID family (ID1, ID2, ID3), the cyclin-dependent kinase inhibitor CDKN1A (p21), the pro-apoptotic BAX, and the transcription factor JUNB. Signaling is modulated by interacting proteins such as SMURF1, FKBP12, and endoglin, and converges with TGF-beta, MAPK/ERK, and Wnt pathways.

In the colorectum, BMPR1A acts as a tumor suppressor by promoting differentiation and apoptosis while suppressing stem cell self-renewal. Its inactivation is implicated in juvenile polyposis syndrome and contributes to colorectal and gastric cancer progression. The HCT 116 knockout model thus enables dissection of BMPR1A-mediated tumor suppression in a background of concurrent oncogenic mutations.

This polyclonal knockout cell population supports diverse applications, including mechanistic studies of BMP tumor suppressor signaling in colorectal cancer, functional modeling of juvenile polyposis syndrome, drug screening for BMP pathway modulators, and investigation of intestinal stem cell dynamics. Common assays include Western blotting for phospho-SMAD1/5/8, RT-qPCR of ID1/ID2, BRE-luciferase reporter, cell proliferation and apoptosis (cleaved caspase-3) assays, immunofluorescence for SMAD4 nuclear translocation, colony formation, and xenograft tumor growth. For additional information, please contact Ascent Research.

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