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Cat. No. ARG31975

C1GALT1 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

CRISPR/Cas9-edited polyclonal knockout cell population of human A-549 lung adenocarcinoma cells with targeted disruption of the C1GALT1 gene. C1GALT1 encodes the core 1 galactosyltransferase that, with its chaperone Cosmc, initiates mucin-type O-glycosylation on substrates including MUC1, IgA1, and Notch receptors. Its knockout leads to Tn antigen exposure, providing a model for aberrant glycosylation in cancer, Tn syndrome, and IgA nephropathy. Host A-549 cells are a widely used alveolar type II epithelial model enabling glycobiology, oncology, and respiratory research. This product is suitable for lectin-based phenotyping, Notch signaling assays, and functional studies of O-glycan-dependent processes. Contact Ascent Research for further information.

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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

    C1GALT1

    Gene Identifier

    NCBI Gene ID 56913

    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 C1GALT1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the human A-549 lung adenocarcinoma cell line, providing a loss-of-function model for the core 1 ??1,3-galactosyltransferase (C1GALT1) gene. The polyclonal format yields a heterogeneous cell pool with target-gene disruption, well-suited for pooled functional screening and glycobiology applications.

A-549 is an adherent epithelial-like cell line derived from a 58-year-old Caucasian male with lung adenocarcinoma, serving as a model of alveolar type II epithelium. It is extensively used in respiratory biology, oncology, and pharmacological research due to its robust signaling characteristics and ease of genetic modification.

C1GALT1, together with its obligate chaperone C1GALT1C1 (Cosmc), catalyzes the transfer of galactose to GalNAc-O-Ser/Thr to form core 1 O-glycans (T-antigen) on glycoproteins such as MUC1, IgA1, Notch receptors, ??1 integrins, and CD44. Its transcription is positively regulated by SP1. Knockout of C1GALT1 ablates core 1 synthesis, resulting in truncated Tn antigen exposure, which disrupts glycoprotein stability, cell adhesion, and Notch signaling. This alteration mimics disease-relevant glycosylation defects observed in Tn syndrome, IgA nephropathy, and cancers with aberrant O-glycosylation.

In the A-549 background, C1GALT1 knockout enables the study of mucin-type O-glycosylation in lung adenocarcinoma epithelium. It provides a system to examine how Tn antigen accumulation affects key oncogenic processes such as MUC1-mediated signaling, integrin-dependent adhesion, and Notch pathway activity, thereby offering insights into glycosylation-dependent mechanisms of tumor progression and immune recognition.

Key applications include glycobiology of cancer, O-glycan biosynthesis, IgA nephropathy modeling, Notch signaling studies, and congenital disorders of glycosylation. Common assays involve lectin blotting with PNA and VVA, flow cytometry with lectins, MUC1 Western blot, RT-qPCR, cell adhesion assays, and Notch reporter assays. For additional product details, please contact Ascent Research.

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