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Cat. No. ARG36062

KCNK3 Knockout HCT116 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Large intestine (colon)

  • Disease:

    Carcinoma

KCNK3 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the KCNK3 gene in human colorectal carcinoma HCT 116 cells. KCNK3 encodes the TASK-1 background potassium channel, which is sensitive to pH, hypoxia, and regulation by G-protein coupled receptors, protein kinase A, and protein kinase C. This knockout model enables dissection of KCNK3-dependent signaling in cancer cell biology, including its influence on voltage-gated calcium channels, cell proliferation, and apoptosis. Suitable for electrophysiological recording, membrane potential assays, calcium imaging, and drug screening studies.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HCT 116

    Sex of Donor

    Male

    Age

    Adult

    Derived From Site

    In situ; Colon

    Gene Name

    KCNK3

    Gene Identifier

    NCBI Gene ID 3777

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    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

KCNK3 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with targeted disruption of the KCNK3 gene in human HCT 116 colorectal carcinoma cells. This heterogeneous pool of edited cells enables loss?of?function studies without clonal selection bias, providing a robust model for investigating the roles of the TASK?1 background potassium channel in epithelial cancer cell physiology.

The HCT 116 cell line is a widely used model of colorectal adenocarcinoma derived from a human male. These epithelial cells retain key oncogenic signaling pathways (e.g., Wnt, MAPK, PI3K) and are highly proliferative, making them suitable for studying cell cycle regulation, apoptosis, and drug sensitivity. Their genetic tractability facilitates efficient CRISPR/Cas9 genome editing to create knockout models for cancer research.

KCNK3 encodes TASK?1, a pH? and hypoxia?sensitive two?pore domain potassium channel that regulates resting membrane potential and cellular excitability. Its activity is controlled by upstream factors including G?protein coupled receptors (e.g., 5?HT receptors), PKA, PKC, and anesthetics. Channel inhibition, triggered by G??q?coupled signals or acidosis, induces membrane depolarization, opening voltage?gated calcium channels (CaV1.2) and elevating intracellular Ca2?. This calcium influx, mediated in part by 14?3?3 proteins and syntaxin, influences downstream processes such as proliferation and apoptosis. KCNK3 also heterodimerizes with TASK?3, affecting channel trafficking. Consequently, TASK?1 integrates signals from cAMP?PKA, phospholipase C, and calcium pathways to modulate cellular responses.

In HCT 116 cells, KCNK3 disruption allows dissection of its contributions to membrane potential dynamics, calcium signaling, and cancer cell behavior, particularly under hypoxia or altered pH conditions typical of the tumor microenvironment. The polyclonal knockout captures heterogeneous editing outcomes, better reflecting tumor genetic variability. This model also aids understanding of KCNK3??s role in diseases like pulmonary arterial hypertension and cardiac arrhythmias, expanding its utility beyond oncology.

This product supports diverse assays: western blotting and RT?qPCR for knockout validation, immunofluorescence for channel localization, patch?clamp electrophysiology for potassium current recording, and membrane potential or calcium imaging for functional analyses. Phenotypic assays for proliferation, apoptosis, and migration/invasion are also applicable. It is well?suited for drug screening targeting K2P channels and for basic research into ion channel?mediated signaling in epithelial cancers. For further details, contact Ascent Research.

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