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Cat. No. ARG43259

CCNT1 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The CCNT1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-generated polyclonal knockout population in the MES-OV ovarian endometrioid carcinoma line, disrupting cyclin T1, the regulatory subunit of P-TEFb. Cyclin T1 partners with CDK9 to phosphorylate RNA Pol II CTD Ser2 and negative elongation factors, driving transcriptional elongation, which is dysregulated in HIV-1 Tat transactivation and ovarian cancer. These cells enable functional studies such as ChIP-qPCR, RNA-seq, HIV-1 LTR-luciferase assays, and CDK9 inhibitor screening. Disruption of CCNT1 allows dissection of P-TEFb-dependent transcriptional networks and evaluation of cyclin T1 as a therapeutic target in epithelial ovarian cancer.

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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

    CCNT1

    Gene Identifier

    NCBI Gene ID 904

    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 CCNT1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited bulk population of MES-OV human ovarian endometrioid carcinoma cells, in which the CCNT1 gene has been disrupted to create a loss-of-function model for cyclin T1. As a polyclonal knockout pool, these cells provide a genetically heterogeneous background that facilitates the study of CCNT1-dependent functions without clonal artifacts. This knockout product is particularly suited for investigating the role of cyclin T1 in transcriptional elongation, P-TEFb complex activity, and the regulatory networks that control RNA polymerase II pause release.

The MES-OV cell line originates from a human ovarian endometrioid adenocarcinoma and displays an adherent epithelial morphology, representing a well-characterized model of epithelial ovarian cancer. This cell line supports reproducible growth and is suitable for diverse assays, including drug sensitivity, proliferation, and migration analyses. Its ovarian endometrioid carcinoma background offers a clinically relevant system for investigating gene dysregulation and evaluating targeted therapeutics in this cancer subtype.

Cyclin T1 (CCNT1) is the regulatory subunit of P-TEFb, forming an active kinase complex with CDK9 that phosphorylates Ser2 of the RNA polymerase II CTD and negative elongation factors NELF-E and SPT5, facilitating productive transcriptional elongation. P-TEFb is regulated by reversible incorporation into the 7SK snRNP (containing HEXIM1 and LARP7), from which it can be released by BRD4. In ovarian cancer cells, MAPK/ERK signaling converges on P-TEFb to control immediate early gene expression. Additionally, HIV-1 Tat directly binds cyclin T1 to hijack P-TEFb for viral LTR transactivation.

Disruption of CCNT1 in MES-OV cells provides a unique model to study the role of transcriptional elongation in ovarian endometrioid carcinoma. Loss of cyclin T1 can reveal P-TEFb-dependent oncogenic programs and help dissect interactions with tumor-suppressive PML nuclear bodies. Moreover, this polyclonal knockout enables HIV-1 Tat transactivation studies in an epithelial context, broadening the utility for mechanistic investigations and inhibitor screening.

Typical applications include ChIP-qPCR for RNA Pol II occupancy, RNA-seq for transcriptome profiling, HIV-1 LTR-luciferase reporter assays, and cell-based functional assays such as proliferation, migration, and sensitivity to CDK9 inhibitors. These polyclonal knockout cells are well suited for high-throughput screening of P-TEFb-targeting compounds and for deciphering cyclin T1??s role in ovarian cancer biology. For further inquiries, please contact Ascent Research.

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