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Cat. No. ARG35545

GYS1 Knockout DLD-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Large intestine (colon)

  • Disease:

    Adenocarcinoma

The GYS1 Knockout DLD-1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population derived from the DLD-1 human colorectal adenocarcinoma cell line. This model disrupts glycogen synthase 1 (GYS1), the rate-limiting enzyme in glycogen synthesis, within a clinically relevant colorectal cancer background. GYS1 activity is controlled by upstream regulators including AKT and GSK3??, and its disruption enables investigation of glycogen metabolism, cancer metabolic reprogramming, and glycogen storage diseases using assays such as PAS staining, western blotting, and Seahorse flux analysis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    DLD-1

    Age

    Adult

    Gene Name

    GYS1

    Gene Identifier

    NCBI Gene ID 2997

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 GYS1 Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population generated from the DLD-1 human colorectal adenocarcinoma cell line, with targeted disruption of the GYS1 gene. This loss-of-function model delivers a heterogeneous cellular background for investigating glycogen synthase 1 function, avoiding the limitations of single-cell clonal expansion.

The parental DLD-1 line is a widely used human colorectal adenocarcinoma model, originally isolated from a male patient, displaying epithelial morphology. It is a standard tool in colorectal cancer research, particularly for studies of tumor metabolism, signaling transduction, and therapeutic interventions.

The gene product GYS1, glycogen synthase 1, is the rate-limiting enzyme for glycogen synthesis, catalyzing the transfer of glucose from UDP-glucose to a growing glycogen chain initiated by glycogenin (GYG1). The enzyme is regulated by phosphorylation: GSK3??, AMPK, and PKA inactivate it, while PP1-dependent dephosphorylation activates it. Insulin/IGF1 signaling promotes activation via AKT-mediated inhibition of GSK3??. GYS1 interacts with GYG1, PPP1R3C, GBE1, laforin, and malin, and directs glycogen production, thereby modulating glucose-1-phosphate, glucose-6-phosphate, and cellular energy reserves.

In the DLD-1 colorectal adenocarcinoma setting, GYS1 disruption permits dissection of glycogen synthesis contributions to cancer cell metabolism. Colorectal tumors often exhibit altered energy storage and metabolic reprogramming, making this knockout model valuable for probing GYS1-driven effects on proliferation, survival, and adaptation. It is particularly suited to study metabolic dependencies, potential roles in cachexia, and glycogen storage disease mechanisms.

This polyclonal knockout cell population supports diverse experimental applications, including cellular metabolism studies, cancer metabolic reprogramming analysis, and glycogen storage disease modeling. Common assay modalities include PAS staining for glycogen quantitation, western blotting for GYS1 and phospho-GYS1, glucose uptake assays, Seahorse metabolic flux profiling, proliferation assays (MTT/BrdU), colony formation tests, and RT-qPCR for metabolic gene expression. For additional technical details or ordering assistance, please contact Ascent Research.

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