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Cat. No. ARG35785

KCNK3 Knockout A2780 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Endometrioid carcinoma

KCNK3 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human KCNK3 gene in the A2780 ovarian cancer cell line. KCNK3 encodes the pH- and hypoxia-sensitive potassium channel TASK-1, which regulates resting membrane potential and cellular excitability through interactions with protein kinase A, ERK1/2, and NFAT signaling. This loss-of-function model is ideal for studying TASK-1's role in ovarian cancer proliferation, hypoxia sensing, and tumor microenvironment adaptation. Applications include patch-clamp electrophysiology, membrane potential assays, viability/apoptosis studies, and drug screening for TASK-1 modulators.

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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

    KCNK3

    Gene Identifier

    NCBI Gene ID 3777

    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

KCNK3 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the human KCNK3 gene. These polyclonal knockout cells are generated by CRISPR/Cas9-mediated gene disruption, ensuring a loss-of-function model without clonal isolation. This heterogeneous pool enables robust functional analysis of TASK-1 potassium channel function in an ovarian cancer context.

The A2780 host cell line is a human epithelial ovarian carcinoma cell line established from an untreated patient, serving as a well-characterized model for high-grade serous ovarian cancer. Its tumorigenic properties and sensitivity to chemotherapeutics make it widely used in oncogenic signaling and drug response studies, owing to its well-documented epithelial origin and relevance to ovarian carcinoma research.

KCNK3 encodes TASK-1, a pH- and hypoxia-sensitive potassium leak channel that sets the resting membrane potential. Its activity is modulated by extracellular pH, oxygen tension, protein kinase A, angiotensin II, and inhalational anesthetics. Channel opening hyperpolarizes the membrane, influencing calcium signaling, ERK1/2 phosphorylation, NFAT activation, and cell cycle progression. TASK-1 interacts with 14-3-3??, arrestin-2, SUMO1, and forms heterodimers with TASK-3. Within the hypoxia?CHIF-1???CcAMP?CPKA?CERK1/2 axis, TASK-1 serves as a critical sensor linking microenvironmental changes to cellular outcomes.

In A2780 cells, KCNK3 knockout disrupts potassium conductance, altering membrane potential and impairing responses to pH and hypoxia. This may impact proliferation, apoptosis, and tumor microenvironment sensing, as TASK-1 contributes to adaptive mechanisms under acidic and hypoxic stress. This polyclonal model is valuable for studying KCNK3’s role in ovarian carcinoma survival, migration, and chemoresistance, and for dissecting pH homeostasis in the tumor niche.

Applications include patch-clamp electrophysiology, membrane potential assays, and Western blot/RT-qPCR for confirming disruption. Viability (MTT) and apoptosis (Annexin V) assays can be performed alongside hypoxia chamber experiments to probe hypoxia-dependent phenotypes. Migration/invasion assays and drug screening for TASK-1 modulators are also relevant, with implications for ovarian cancer and pulmonary arterial hypertension research. For further information, contact Ascent Research.

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