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Cat. No. ARG36707

ASRGL1 Knockout SKOV3 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

The ASRGL1 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to model loss of ASRGL1 function in a p53-mutant ovarian cancer background. ASRGL1 is an asparaginase that depletes extracellular asparagine, suppressing mTORC1 and inducing apoptosis; its expression is transcriptionally regulated by p53 and the GCN2-ATF4 stress pathway. These cells enable investigation of asparagine metabolism, chemoresistance, and mTOR signaling in ovarian cancer, with applications including Western blotting, RT-qPCR, viability assays, and xenograft studies. Key pathway partners include mTORC1, ATF4, and PIMT.

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Shipping Info:

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

    ASRGL1

    Gene Identifier

    NCBI Gene ID 80150

    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 ASRGL1 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-OV-3 human ovarian adenocarcinoma cell line. Using CRISPR/Cas9-mediated gene disruption, the ASRGL1 locus is targeted to abolish its enzymatic activity. This product offers a loss-of-function model for investigating ASRGL1 (asparaginase-like 1) in cancer biology. The polyclonal format maintains genetic diversity, supporting pooled functional studies, drug screening, and pathway analysis.

SK-OV-3 is a widely used epithelial ovarian cancer cell line from patient ascites, with mutant p53 and inherent chemoresistance. It serves as a key model for ovarian cancer progression, drug resistance, and metastasis. Its p53 deficiency is crucial because p53 transcriptionally activates ASRGL1, enabling investigation of ASRGL1 in a p53-mutant background that reflects clinical tumors.

ASRGL1 encodes a cytoplasmic L-asparaginase that hydrolyzes asparagine to aspartic acid and ammonia, depleting extracellular asparagine and suppressing mTORC1 signaling. Its expression is activated by p53 and nutrient stress via the GCN2-ATF4 pathway. Loss of ASRGL1 leads to mTORC1 hyperactivity, reduced apoptosis, and cell cycle progression. The enzyme functions as a homodimer and interacts with substrates L-asparagine and isoaspartyl peptides, as well as with PIMT for protein repair via its isoaspartyl peptidase activity. Key pathway components include ASNS, GCN2, mTORC1, ATF4, and PIMT.

In SK-OV-3 cells lacking wild-type p53, ASRGL1 dysregulation may promote asparagine addiction and chemoresistance. This polyclonal knockout population enables study of ASRGL1 loss on asparagine metabolism, mTORC1 activity, and stress survival without clonal selection bias. The model is valuable for investigating apoptosis, metabolic vulnerabilities, and tumor progression mechanisms in p53-mutant ovarian cancers.

Researchers can apply this product in Western blotting (ASRGL1, mTOR pathway markers such as phospho-S6K), RT-qPCR (ASRGL1, ATF4, CHOP), asparaginase activity assays, cell viability/proliferation assays, apoptosis detection by Annexin V/PI flow cytometry, metabolomic profiling of asparagine/aspartate, and xenograft tumor models to evaluate therapeutic responses. For further details or to request a quote, please contact Ascent Research.

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