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Cat. No. ARG37446

ABHD14B Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The ABHD14B Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population for studying ABHD14B, a putative lysine deacetylase that interacts with calmodulin (CALM1/CALM2/CALM3). This loss-of-function model in HeLa cervical adenocarcinoma cells enables functional dissection of the molecular link between calcium signaling and protein deacetylation. Applications include investigating acetylation-dependent regulation of cell proliferation and apoptosis, calcium-dependent signaling, and protein acetylation dynamics. Typical assays comprise Western blotting for acetylated proteins, co-immunoprecipitation of ABHD14B-calmodulin complexes, and cell viability assays, supporting cancer biology research and therapeutic target validation.

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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

    ABHD14B

    Gene Identifier

    NCBI Gene ID 84836

    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 ABHD14B Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population carrying targeted disruption of the ABHD14B gene. This product constitutes a loss-of-function model for investigating ABHD14B, an alpha/beta hydrolase domain-containing protein with putative lysine deacetylase activity. The polyclonal knockout approach provides a heterogeneous pool of edited cells, enabling robust functional genomics studies and bulk assays without the limitations of single-cell clones. Researchers can utilize this system to examine ABHD14B-dependent molecular mechanisms in a controlled genetic context.

The host HeLa cell line is a human cervical adenocarcinoma epithelial model, positive for HPV18, with p53 and retinoblastoma protein (Rb) inactivated by the viral E6 and E7 oncoproteins, respectively. This well-characterized cancer cell line is widely employed in studies of cervical cancer biology, signal transduction, and gene function. Its defined genetic background and reproducible growth characteristics make it an ideal platform for dissecting pathways involved in proliferation, apoptosis, and transformation.

ABHD14B is a member of the alpha/beta hydrolase superfamily and encodes a putative lysine deacetylase that binds directly to calmodulin (CALM1/CALM2/CALM3). This interaction positions ABHD14B at the interface of calcium signaling and protein deacetylation, presumably functioning downstream of calcium/calmodulin activation. The enzyme is believed to target specific deacetylated protein substrates, potentially histones or non-histone proteins, thereby modulating acetylation-dependent processes such as gene expression and protein stability. The calmodulin-ABHD14B-substrate axis represents a putative mechanism linking calcium fluxes to the cellular acetylome.

In the HeLa cervical cancer context, ABHD14B knockout permits functional dissection of its role in acetylation-mediated regulation of cell proliferation and apoptosis. With p53 and Rb pathways already disrupted, this model is valuable for evaluating whether ABHD14B exerts tumor-suppressive or oncogenic functions. It enables identification of ABHD14B-dependent acetylation changes on key regulatory proteins and assessment of their impact on cellular responses to calcium. Moreover, the system can be used to test sensitivity to deacetylase inhibitors in a cancer-relevant background.

Applications include functional characterization of ABHD14B deacetylase activity, investigation of calcium-dependent signaling cascades, and analysis of protein acetylation dynamics. Typical assays involve Western blotting for acetylated proteins, co-immunoprecipitation to confirm calmodulin binding, cell viability and apoptosis assays, calcium imaging, and deacetylase enzymatic measurements. The polyclonal knockout pool is also suited for CRISPR-based screens and downstream target validation. For further technical details, please contact Ascent Research.

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