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Cat. No. ARG35647

ALDH1B1 Knockout 143B Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Osteosarcoma

The ALDH1B1 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human osteosarcoma 143B line, providing a loss-of-function model for the mitochondrial aldehyde dehydrogenase ALDH1B1. This enzyme catalyzes retinaldehyde oxidation to retinoic acid, is regulated by Wnt/??-catenin/TCF/LEF and retinoic acid, and influences differentiation and stemness via RAR/RXR and HOX genes. Applications include cancer stem cell phenotyping, retinoic acid signaling analysis, Wnt pathway dissection, and metabolic detoxification studies, using techniques such as ALDH activity assays, LC-MS, RT-qPCR, and flow cytometry.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    143B

    Age

    13 years

    Gene Name

    ALDH1B1

    Gene Identifier

    NCBI Gene ID 219

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM/F12

    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 ALDH1B1 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-mediated gene disruption product, offering a polyclonal knockout cell population derived from the human osteosarcoma cell line 143B. This heterogeneous pool exhibits targeted loss of ALDH1B1 function, providing researchers with a versatile and ready-to-use loss-of-function model. The polyclonal format averages clonal variation and simplifies experimental workflows by eliminating the need for single-cell isolation, making it suited for rapid phenotype screening and pathway analysis.

The host 143B cell line is a well-characterized human osteosarcoma model established from a biopsy of a grade-3 bone tumor. It displays aggressive proliferation, high tumorigenicity, and a propensity for metastasis in vivo, making it a gold standard for osteosarcoma research. The adherent, epithelial-like morphology and stable karyotype facilitate reproducible gene editing, knockdown, and knockout experiments.

ALDH1B1 encodes a mitochondrial aldehyde dehydrogenase that catalyzes the irreversible oxidation of retinaldehyde to all-trans-retinoic acid, utilizing NAD+ as a cofactor. This enzyme is a direct transcriptional target of the Wnt/??-catenin pathway, with ??-catenin/TCF/LEF complexes binding its promoter to drive expression; additional regulation is exerted by retinoic acid, the oxidative stress sensor NRF2, and the nuclear receptor PPAR??. The retinoic acid product functions as a ligand for heterodimeric RAR/RXR nuclear receptors, which translocate to the nucleus and modulate the expression of HOX genes, thereby controlling cell fate decisions, proliferation, and apoptosis. ALDH1B1 also participates in alcohol metabolism by detoxifying acetaldehyde, and its activity has been linked to the preservation of cancer stem cell traits through crosstalk with Wnt/??-catenin signaling, highlighting its dual role in metabolism and stemness.

In the osteosarcoma context, ALDH1B1 knockout allows rigorous examination of how loss of aldehyde dehydrogenase activity impacts retinoic acid biosynthesis, Wnt pathway output, and stem-like cell populations. Because 143B cells are known to harbor subpopulations with stem cell characteristics, the polyclonal knockout is especially useful for identifying ALDH1B1-dependent heterogeneous responses in differentiation, chemoresistance, and tumorigenicity. This model enables the dissection of ALDH1B1??s contribution to osteosarcoma progression and its potential as a therapeutic vulnerability.

This product is ideal for a range of experimental applications, including cancer stem cell analysis via colony formation assays and flow cytometric detection of surface markers, retinoic acid signaling studies through LC-MS-based quantification and RT-qPCR of downstream targets such as RAR?? and HOX genes, and Wnt pathway investigation using Western blotting for ??-catenin and transcriptional activity assays. Additional uses encompass aldehyde dehydrogenase enzymatic assays, acetaldehyde detoxification studies, and drug metabolism screening. For detailed product information or technical assistance, please contact Ascent Research.

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