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Cat. No. ARG37458

ADPGK Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The ADPGK Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from HeLa cells, featuring disruption of the ADPGK gene. This knockout model impairs ADP-dependent glucose phosphorylation, a key alternative glycolytic pathway regulated by HIF-1?? and critical under low ATP conditions. These cells are suitable for investigating cancer metabolism, hypoxia-induced metabolic rewiring, and drug target validation via functional assays including glucose uptake, lactate measurement, Seahorse analysis, and hypoxia viability testing. The HeLa host cell line offers a robust platform for metabolic studies in cervical cancer.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    ADPGK

    Gene Identifier

    NCBI Gene ID 83440

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    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 ADPGK Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells with targeted disruption of the ADPGK gene. This product provides a heterogeneous loss-of-function model, avoiding clonal selection artifacts, suitable for metabolic research applications.

HeLa cells are an HPV18-immortalized human cervical adenocarcinoma epithelial line established in 1951, widely used in cancer biology for their rapid growth and well-characterized metabolic profile. As a cervical cancer model, HeLa cells exhibit high glycolytic activity and are commonly employed to study tumor metabolism and hypoxia responses, providing a relevant host for ADPGK knockout studies.

ADPGK encodes an ADP-dependent glucokinase that phosphorylates glucose to glucose-6-phosphate using ADP as a phosphate donor, enabling glycolysis under ATP-limited conditions. Its expression is induced by HIF-1?? and modulated by PI3K/AKT signaling and glucose deprivation. The enzyme requires magnesium cofactors and generates glucose-6-phosphate, which feeds glycolysis and the pentose phosphate pathway, producing lactate, NADPH, and ribose-5-phosphate. ADPGK interacts within a metabolic network including HK2, G6PD, PGD, TKT, PFKL, PKM2, LDHA, and MCT4. Knockout of ADPGK disrupts this alternative glycolytic route, reducing glycolytic flux and pentose phosphate pathway activity under metabolic stress.

In HeLa cells, ADPGK loss impairs metabolic adaptation during hypoxia and ATP depletion, as the alternative phosphorylation pathway is critical for maintaining energy and biosynthetic precursors. This sensitization highlights a metabolic vulnerability in cancer cells, making the knockout model valuable for probing hypoxia-induced metabolic reprogramming and identifying targets for anti-cancer therapies.

These polyclonal knockout cells are suited for cancer metabolism studies, hypoxia adaptation research, and metabolic drug target validation. Common assays include Western blotting, RT-qPCR, glucose uptake and lactate production measurements, Seahorse extracellular flux analysis, cell viability under hypoxia, metabolomic profiling, and RNA-seq. The mixed population format also supports high-throughput screening for metabolic modulators. For further technical details or experimental design support, please contact Ascent Research.

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