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Cat. No. ARG31910

B4GALT7 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The B4GALT7 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal A-549 lung adenocarcinoma cell population with disrupted B4GALT7. This gene encodes a galactosyltransferase essential for heparan sulfate and chondroitin sulfate biosynthesis, acting downstream of XYLT1/2 and upstream of B3GAT3, regulated by SP1, TGF-??, and NRF2. Knockout impairs glycosaminoglycan assembly on proteoglycans, disrupting FGF2, VEGF, and Wnt signaling and extracellular matrix function. Applications include studies of glycosaminoglycan biology, cancer cell adhesion/invasion, and Ehlers-Danlos syndrome using western blotting, immunofluorescence, and HPLC-MS.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A549

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    Lung

    Gene Name

    B4GALT7

    Gene Identifier

    NCBI Gene ID 11285

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    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 B4GALT7 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human A-549 lung carcinoma cell line, featuring targeted disruption of the B4GALT7 gene. This gene encodes beta-1,4-galactosyltransferase 7, which initiates glycosaminoglycan chain synthesis. The polyclonal format provides a heterogeneous pool of loss-of-function cells, ideal for studying gene function without clonal biases.

A-549 cells, isolated from human lung adenocarcinoma tissue, display adherent epithelial morphology and are extensively used in respiratory research, toxicology, and cancer biology. Their robust expression of proteoglycans and well-mapped signaling pathways make them a relevant host for investigating glycosylation-dependent processes in lung cancer.

B4GALT7 catalyzes the transfer of galactose from UDP-galactose to the xylose residue of the proteoglycan linker region, a reaction dependent on Mn2+. It operates downstream of xylosyltransferases (XYLT1/2) and upstream of B3GAT3. The enzyme is regulated by SP1, TGF-?? signaling, and NRF2. Its activity is essential for the assembly of heparan sulfate, chondroitin sulfate, and dermatan sulfate chains on core proteoglycans, including syndecans and glypicans. These glycosaminoglycan chains serve as co-receptors for growth factors like FGF2, VEGF, and Wnt morphogens, influencing signaling cascades such as ERK and AKT pathways. Consequently, B4GALT7 knockout disrupts glycosaminoglycan biosynthesis, impairing extracellular matrix organization and growth factor signaling.

In the A-549 background, B4GALT7 disruption provides a model to dissect the contribution of glycosaminoglycans to lung adenocarcinoma cell adhesion, invasion, and mitogenic signaling. Loss of heparan sulfate compromises syndecan- and glypican-mediated growth factor presentation, leading to attenuated responses to FGF2 and altered VEGF/Wnt signaling. This system also enables investigation of disease mechanisms underlying Ehlers-Danlos syndrome and other congenital disorders of glycosylation in a cancer-relevant context.

Researchers can utilize these cells in western blotting for core proteoglycans, immunofluorescence detection of heparan sulfate, HPLC-MS disaccharide profiling, cell adhesion and migration assays, and phospho-ERK/AKT analysis. Additional applications include qPCR quantification of glycosyltransferase expression and functional rescue studies. The polyclonal knockout population is well-suited for population-level analyses, drug screening, and genetic interaction studies. For further technical information, please contact Ascent Research.

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