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Cat. No. ARG39048

DNAH5 Knockout MES-OV Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

DNAH5 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the DNAH5 gene in the MES-OV human ovarian clear cell carcinoma line. DNAH5 encodes an axonemal dynein heavy chain that powers ciliary beating and interacts with DNAI1/DNAI2 within the outer dynein arm complex. This knockout model enables investigation of ciliary motility defects and cilia-dependent signaling, including Hedgehog transduction. Key applications include studying primary ciliary dyskinesia, mucociliary clearance, and ciliary roles in ovarian cancer progression using assays such as immunofluorescence, ciliary beat frequency analysis, and migration assays.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    MES-OV

    Sex of Donor

    Female

    Age

    53 years

    Derived From Site

    Ascites

    Gene Name

    DNAH5

    Gene Identifier

    NCBI Gene ID 1767

    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

The DNAH5 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from MES-OV, an ovarian clear cell carcinoma line, with targeted disruption of the DNAH5 gene. This heterogeneous pool contains diverse knockout genotypes, reducing clonal bias and enabling robust population-level functional studies. The gene disruption generates a loss-of-function model for dissecting DNAH5-dependent biological processes.

The MES-OV host cell line originates from a human ovarian clear cell carcinoma, an epithelial cancer subtype characterized by distinct molecular features. It serves as a clinically relevant in vitro model for investigating ovarian cancer biology, including mechanisms of metastasis, drug resistance, and tumor microenvironment interactions.

DNAH5 encodes an outer dynein arm heavy chain essential for ciliary and flagellar motility. Its transcription is regulated by FOXJ1 and RFX transcriptional factors (RFX2, RFX3). The DNAH5 protein interacts with DNAI1, DNAI2, and DNAL1 to form the force-generating dynein complex, driving ATP-dependent microtubule sliding and ciliary beat. Downstream, ciliary motility underpins mucociliary clearance, cerebrospinal fluid flow, and left-right axis determination. In primary cilia, Hedgehog signaling relies on intact ciliary architecture: Hedgehog binding to PTCH1 activates SMO, leading to GLI transcription factor activation. Loss of DNAH5 may impair ciliary motility and potentially alter Hedgehog signal transduction.

Within the ovarian cancer context, ciliary dysfunction has been linked to tumor progression and altered signaling. These DNAH5 knockout MES-OV cells allow dissection of how ciliary beat deficiency influences cancer-relevant phenotypes such as migration, invasion, and response to Hedgehog pathway inhibitors. The model enables correlation of ciliary motility with downstream signaling outputs, including GLI activation, and exploration of crosstalk with Wnt/planar cell polarity pathways, offering insights into cilia-dependent mechanisms in ovarian clear cell carcinoma.

Key applications include studying ciliary biology, modeling primary ciliary dyskinesia, and assessing mucociliary clearance defects. Researchers can employ western blotting for DNAH5 expression, immunofluorescence for cilia markers (acetylated tubulin, ARL13B), ciliary beat frequency measurement by high-speed microscopy, RT-qPCR for ciliogenesis genes, RNA-seq transcriptomics, and functional assays such as cell cycle analysis, apoptosis, and migration/invasion. The polyclonal format supports both targeted mechanistic studies and broader phenotypic screens. For further details or to request a quote, contact Ascent Research.

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