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Cat. No. ARG36757

ABCB10 Knockout T47D Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Breast (mammary gland)

  • Disease:

    Ductal carcinoma

CRISPR/Cas9-edited polyclonal ABCB10 knockout cell population derived from the T-47D human breast cancer cell line, engineered to disrupt the mitochondrial transporter ABCB10, which is critical for heme biosynthesis, iron homeostasis, and oxidative stress protection. This loss-of-function model enables study of mitochondrial transport in a breast cancer context. ABCB10 is regulated by GATA1 and TP53, and interacts with FECH and ALAS2; its knockout allows investigation of downstream effects on HMOX1, SOD2, and cellular redox balance. Ideal for heme quantification, ROS detection, viability, and migration assays, these cells support drug screening and evaluation of ABCB10 as a therapeutic target in hormone-responsive breast cancer.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    T-47D

    Sex of Donor

    Female

    Age

    54 years

    Derived From Site

    Metastatic; Pleural effusion

    Gene Name

    ABCB10

    Gene Identifier

    NCBI Gene ID 23456

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 10μg/mL Insulin, 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 ABCB10 Knockout T-47D Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human breast cancer cell line T-47D, offering a loss-of-function model for the ABCB10 gene. This polyclonal pool contains diverse edited alleles, providing a robust tool for initial functional screening without clonal biases. The gene disruption is achieved via CRISPR/Cas9, enabling researchers to study ABCB10 deficiency in a disease-relevant context.

T-47D is a widely used luminal B breast cancer cell line established from a pleural effusion of a ductal carcinoma patient. These epithelial cells are estrogen receptor (ER)-, progesterone receptor (PR)-, and HER2-positive, and harbor PIK3CA and TP53 mutations, reflecting key features of hormone-responsive breast cancer. The line??s well-characterized molecular landscape makes it suitable for studying gene function in breast cancer biology.

ABCB10 encodes a mitochondrial inner membrane transporter essential for heme biosynthesis and iron homeostasis, and for protection against oxidative stress. Transcription is regulated by GATA1, TP53, and NFE2L2. ABCB10 interacts with ferrochelatase (FECH) and ALAS2 to facilitate heme precursor transport, and functionally relates to ABCB7. Downstream, it modulates expression of HMOX1, SOD2, and FECH, linking mitochondrial transport to antioxidant defenses.

In T-47D cells, ABCB10 disruption likely impairs mitochondrial iron homeostasis and increases oxidative stress susceptibility, potentially affecting tumor cell viability. Since these cells express ER, PR, and HER2, the model enables study of crosstalk between heme metabolism and hormone signaling, and may alter responses to therapies like tamoxifen. This model aids in dissecting the role of mitochondrial transporters in cancer progression and drug resistance.

Applications include investigation of mitochondrial heme transport using heme quantification, mitochondrial iron measurement, and ROS detection assays. The knockout cells support western blotting and RT-qPCR validation of targets (e.g., HMOX1, SOD2) and regulators (e.g., GATA1, TP53), and functional assays such as cell viability, apoptosis, colony formation, and migration. They are suitable for drug screening to target iron addiction or oxidative stress vulnerabilities, and for evaluating ABCB10 as a therapeutic target. For further information, please contact Ascent Research.

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