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Cat. No. ARG39516

DNTTIP1 Knockout A2780 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Endometrioid carcinoma

The DNTTIP1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from human ovarian carcinoma A2780 cells, featuring disruption of DNTTIP1, a regulator of terminal deoxynucleotidyl transferase (TdT) activity in DNA repair and V(D)J recombination. DNTTIP1 interacts with TdT, DNA polymerase mu, and DNA ligase IV, and functions downstream of TP53 in the DNA damage response. This knockout model is suitable for studying DNA repair, ovarian cancer biology, chemoresistance mechanisms, and drug sensitivity using assays such as ??H2AX foci detection and clonogenic survival.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A2780

    Sex of Donor

    Female

    Age

    Unknown

    Derived From Site

    In situ; Ovary

    Gene Name

    DNTTIP1

    Gene Identifier

    NCBI Gene ID 116092

    Morphology

    Epithelial-like

    Growth Mode

    Adherent and suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 DNTTIP1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian carcinoma epithelial cell line A2780, featuring disruption of the DNTTIP1 gene. This polyclonal knockout model provides a heterogeneous pool of edited cells for functional studies of DNTTIP1 in DNA repair and chromatin organization.

The A2780 cell line is a well-established model of human ovarian adenocarcinoma, widely used in ovarian cancer research, particularly in studies of chemoresistance and tumor progression. These epithelial cells retain key characteristics of high-grade serous ovarian carcinoma and are valuable for investigating DNA damage responses and therapeutic vulnerabilities.

DNTTIP1 encodes a protein that directly interacts with terminal deoxynucleotidyl transferase (DNTT/TdT) to regulate template-independent nucleotide addition during non-homologous end joining (NHEJ) and V(D)J recombination. The DNTTIP1 protein functions within the DNA damage response network, interacting with DNA repair factors including DNA polymerase mu and DNA ligase IV. Upstream, TP53 and other DNA damage-responsive transcription factors regulate DNTTIP1 expression. DNTTIP1-mediated control of TdT activity influences DNA repair efficiency and genomic stability, linking this gene to chromatin remodeling and the broader DNA repair machinery involving XRCC4, DNA-PKcs, and Artemis.

In A2780 ovarian cancer cells, DNTTIP1 disruption may impair double-strand break repair, potentially increasing genomic instability and altering sensitivity to DNA-damaging agents. This polyclonal knockout population enables investigation of DNTTIP1-dependent DNA repair mechanisms in a chemoresistant ovarian cancer context, offering a tool to dissect how altered DNA repair pathways contribute to drug resistance and cancer cell survival.

Typical research applications include DNA repair pathway analysis, ovarian cancer biology, chemoresistance mechanism studies, and functional genomics screens. Representative assays include western blotting, immunofluorescence staining of ??H2AX foci, clonogenic survival assays, comet assays, drug sensitivity profiling with cisplatin or PARP inhibitors, and transcriptomic analysis by RNA-seq. For further information or to inquire about this product, please contact Ascent Research.

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