Security Notice: Please be aware of impersonation attempts using our company name
Legitimate communications from Ascent Research will only come from official @ascentresearch.com email addresses.
Quick Order Cart

Cat. No. ARG0291

Miat Knockout HEI-OC1 Cell Line

  • Product Type:

    Genome-edited Cells

  • Disease:

    Normal

  • Gene Species:

    Mus musculus (Mouse)

The Miat Knockout HEI-OC1 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the immortalized mouse cochlear hair cell-like cell line HEI-OC1. Disruption of the long non-coding RNA Miat, a competitive endogenous RNA that regulates apoptosis and proliferation by sponging miR-150 and miR-22, provides a loss-of-function model for auditory research. Miat is regulated by NF-??B, SP1, p53, and TGF-??, and modulates Wnt/??-catenin and NF-??B signaling pathways, controlling Bcl-2 and Bax expression. This cell line is designed for investigating hearing loss mechanisms, ototoxicity screening, and lncRNA functional analysis. Applications include RT-qPCR, western blotting, RNA-seq, flow cytometry, and cell viability assays to study hair cell survival and apoptosis. Contact Ascent Research for further information.

Inquire Now

In stock

Ships next business day


Ask a Question

Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HEI-OC1

    Gene Name

    Miat

    Gene Alias

    myocardial infarction associated transcript

    Gene Species

    Mus musculus (Mouse)

    Gene Identifier

    NCBI Gene ID 330166

    Gene Type

    ncRNA

  • Culture Conditions

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    Daily monitoring confirms that the cells are free from bacterial, yeast, and fungal contamination.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

    Pathogens

    Cells tested negative for HIV-1, HBV, and HCV.

  • 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 Miat Knockout HEI-OC1 Cell Line is a CRISPR/Cas9-edited knockout cell line in which the long non-coding RNA gene Miat has been disrupted using CRISPR/Cas9-mediated gene disruption. Derived from the HEI-OC1 immortalized mouse cochlear hair cell-like cell line, this product provides a powerful loss-of-function model for dissecting the biological functions of Miat in auditory sensory hair cells. The knockout cell line serves as a valuable tool for investigating the role of this lncRNA in cell proliferation, apoptosis, and gene expression regulation within the context of cochlear biology.

The host HEI-OC1 cell line is an immortalized mouse organ of Corti cell line established from H-2Kb-tsA58 transgenic mice (Immortomouse). These cells retain many phenotypic characteristics of auditory sensory hair cells and are widely used as an in vitro model system for studying hair cell biology, ototoxicity, and age-related hearing loss. HEI-OC1 cells respond to ototoxic stimuli such as aminoglycosides and cisplatin, making them a relevant platform for evaluating the cellular and molecular mechanisms underlying hair cell damage and survival.

Miat is a long non-coding RNA that functions as a competitive endogenous RNA (ceRNA), sequestering microRNAs such as miR-150 and miR-22 to regulate apoptosis- and proliferation-related gene expression. Transcription of Miat is activated by NF-??B, SP1, p53, and TGF-?? signaling pathways. The lncRNA interacts with epigenetic modifiers EZH2, SUZ12, and DNMT1, and it modulates components of the Wnt/??-catenin cascade including Wnt3a, ??-catenin, and TCF4, as well as NF-??B pathway members NF-??B p65 and I??B??. Through these interactions, Miat controls the expression of Bcl-2 and Bax, key determinants of cell survival and death.

In HEI-OC1 cells, Miat disruption likely compromises cell survival and apoptotic programs, directly impacting cochlear hair cell function. This loss-of-function model allows researchers to dissect the ceRNA network underlying ototoxic responses and hearing loss, and to evaluate whether restoring Miat-mediated microRNA sponging can protect against hair cell damage.

Applications encompass hearing loss mechanism studies, ototoxicity screening, lncRNA functional analysis, and auditory cell line engineering. Compatible techniques include RT-qPCR, western blotting, RNA-seq, immunofluorescence, flow cytometry, apoptosis and viability assays, luciferase reporter assays, and RNA immunoprecipitation. For further information, please contact Ascent Research.

Reset Password

    Reach Us Questions? Click Me Here!

    Fill out the form below and a member of our team will contact you shortly!

    *Required field



      Reach Us

      Fill out the form below and a member of our team will contact you shortly!

      *Required field

      Product Inquiry (Optional)