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Cat. No. ARG35755

ASGR1 Knockout A2780 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Endometrioid carcinoma

CRISPR/Cas9-edited polyclonal ASGR1 knockout A2780 cells, derived from human ovarian carcinoma, provide a heterogeneous loss-of-function model for studying asialoglycoprotein receptor 1 biology in a non-hepatic context. ASGR1, a C-type lectin that normally mediates endocytosis and lysosomal degradation of desialylated glycoproteins, is disrupted in this cell population, allowing investigation of glycoprotein clearance, lipid metabolism, and receptor trafficking independent of liver-specific factors. These polyclonal knockout cells enable functional assays such as ligand uptake, flow cytometry, and lysosomal activity analysis, and are valuable for drug targeting research, cancer cell biology studies, and mechanistic dissection of ASGR1 interactions with ASGR2, clathrin, and adaptor protein complex 2.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A2780

    Sex of Donor

    Female

    Age

    Unknown

    Derived From Site

    In situ; Ovary

    Gene Name

    ASGR1

    Gene Identifier

    NCBI Gene ID 432

    Morphology

    Epithelial-like

    Growth Mode

    Adherent and suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 ASGR1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the ASGR1 gene has been disrupted within the A2780 human ovarian carcinoma cell line. This product provides a genetically heterogeneous loss-of-function model that bypasses single-cell cloning, thereby preserving population diversity and reducing clonal artifacts. It is specifically designed for applications that require stable, averaged ASGR1 knockout effects across a polyclonal pool.

A2780 is an epithelial ovarian cancer model established from an untreated patient with ovarian endometrioid adenocarcinoma. The cell line exhibits adherent growth, hormone sensitivity, and well-characterized genomic features, making it a versatile platform for cancer biology, drug sensitivity testing, and xenograft studies. Its malignant epithelial context is particularly relevant for exploring how glycoprotein clearance pathways and endocytic trafficking become dysregulated in cancer.

ASGR1 encodes the major subunit of the asialoglycoprotein receptor, a C-type lectin that mediates hepatic clearance of desialylated glycoproteins via clathrin-mediated endocytosis and lysosomal degradation. Transcriptional regulation is controlled by hepatocyte nuclear factor 4 alpha (HNF4A) and sterol regulatory element-binding protein 2 (SREBF2) in response to cholesterol. ASGR1 forms a heterodimer with ASGR2 and recruits clathrin and adaptor protein complex 2 (AP2) for receptor internalization. Downstream, ASGR1 activity influences lysosomal acid lipase, cathepsin D, and cholesterol efflux, thereby linking glycoprotein homeostasis to lipid metabolism.

Disruption of ASGR1 in A2780 cells creates a unique non-hepatic model that uncouples ASGR1 function from its native liver environment. Because ASGR1 is not endogenously expressed in this ovarian line, the knockout provides a clean background for forced expression, reconstitution, or complementation experiments aimed at dissecting structure?Cfunction relationships. This model also enables evaluation of ASGR1-targeted therapeutics, including antibody-drug conjugates or nanoparticle carriers, in a cancer-relevant setting without confounding endogenous receptor activity.

Key research applications include ligand uptake assays with asialoorosomucoid (ASOR) to quantify receptor-mediated endocytosis, immunofluorescence for tracking receptor internalization, and flow cytometry for measuring surface ASGR1 levels following ectopic expression. Lysosomal activity assays can assess degradative capacity, while transcriptomic profiling by RNA-seq reveals global changes in gene expression upon ASGR1 loss. These polyclonal knockout cells further support drug delivery studies targeting the asialoglycoprotein receptor. For additional technical details or to inquire about custom gene editing solutions, please contact Ascent Research.

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