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Cat. No. ARG36706

ASGR1 Knockout SKOV3 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

CRISPR/Cas9-edited ASGR1 knockout SK-OV-3 polyclonal cells provide a loss-of-function model for the asialoglycoprotein receptor subunit ASGR1 in an ovarian adenocarcinoma background. ASGR1, together with ASGR2, mediates clathrin-dependent endocytosis of desialylated glycoproteins, regulated by HNF4A and C/EBP alpha. This polyclonal population is ideal for investigating glycoprotein clearance, receptor-ligand binding dynamics, and ASGR1-targeted drug delivery, and it supports robust assays such as ligand-binding measurements with asialo-orosomucoid, immunofluorescence tracking of receptor internalization, and western blotting for knockout validation. The heterogeneous knockout pool reduces clonal artifacts and is well-suited for cancer glycobiology research.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    SKOV3

    Sex of Donor

    Female

    Age

    64 years

    Derived From Site

    Ascites

    Gene Name

    ASGR1

    Gene Identifier

    NCBI Gene ID 432

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 SK-OV-3 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population derived from SK-OV-3 human ovarian adenocarcinoma cells, with targeted disruption of the ASGR1 gene encoding the asialoglycoprotein receptor major subunit. This heterogeneous pool harbors diverse loss-of-function mutations at the ASGR1 locus, offering a robust loss-of-function model while minimizing clonal artifacts. Ideal for glycobiology and oncology research, this polyclonal format provides a population-level readout of ASGR1-dependent processes.

SK-OV-3 is an epithelial ovarian cancer cell line originally isolated from ascitic fluid of a patient with ovarian serous cystadenocarcinoma. Widely used to study metastasis, drug resistance, and tumor biology, these cells retain molecular hallmarks of high-grade serous carcinoma. Their epithelial origin and relevance to ovarian cancer make them a suitable host for investigating glycoprotein metabolic pathways in a non-hepatic oncogenic milieu.

ASGR1 encodes the major subunit of the asialoglycoprotein receptor, which hetero-oligomerizes with ASGR2 to recognize desialylated glycoproteins via terminal galactose or GalNAc residues. Ligand binding activates clathrin-dependent endocytosis mediated by the AP-2 adaptor and dynamin, directing cargo through Rab5+ early endosomes to lysosomes for degradation. Its transcription is driven by HNF4A, C/EBP alpha, and FOXA2, embedding ASGR1 within hepatocyte nuclear factor networks. The receptor??s function is calcium-dependent and modulated by ligands like asialo-orosomucoid; downstream, it ensures efficient glycoprotein clearance and, in some contexts, contributes to regulated exocytosis.

Disrupting ASGR1 in SK-OV-3 cells provides a unique model to study glycoprotein turnover in ovarian cancer, where altered glycosylation patterns promote metastasis and immune evasion. The knockout uncouples ASGR1-mediated endocytosis from other trafficking pathways, enabling investigation of desialylated glycoprotein accumulation and its tumorigenic consequences. This system is valuable for testing ASGR1-targeted drug delivery and for probing receptor biology in a non-hepatic environment that possesses the necessary endocytic machinery. Additionally, it allows exploration of ectopic ASGR1 function and its interplay with ovarian cancer cell signaling.

Applications of this knockout product extend across biochemical and cell-based assays, including ligand-binding experiments with asialo-orosomucoid, immunofluorescence visualization of clathrin-mediated internalization, and flow cytometry to confirm surface ASGR1 depletion. The polyclonal population is suitable for co-immunoprecipitation studies to assess ASGR2 complex integrity and for endocytosis assays with fluorescent glycoprotein probes. Validation by RT-qPCR and western blotting ensures loss of ASGR1 expression, while functional assays can investigate alterations in glycoprotein catabolism and downstream effects on ovarian cancer drug sensitivity. For further details, technical assistance, or custom requests, please reach out to Ascent Research.

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