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Cat. No. ARG39707

DPP9 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The DPP9 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from human cervical adenocarcinoma HeLa cells, offering a loss-of-function model for the DPP9 serine protease. DPP9 cleaves N-terminal dipeptides and is implicated in immune regulation, apoptosis, and peptide hormone metabolism. Key substrates include neuropeptide Y (NPY) and glucagon-like peptide-1 (GLP-1), with signaling through IFN-??/NF-??B and interaction with DPP8. These cells are ideal for cancer biology, drug target validation, and protease function studies using enzymatic assays, western blot, and cytokine profiling.

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Shipping Info:

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

    DPP9

    Gene Identifier

    NCBI Gene ID 91039

    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 DPP9 Knockout HeLa Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the DPP9 gene. This loss-of-function model enables investigation of DPP9-dependent processes in an epithelial cervical adenocarcinoma background. The polyclonal format preserves heterogeneous gene-editing outcomes while uniformly eliminating DPP9 protease activity across the pool, providing a robust tool for studying dipeptidyl peptidase 9 biology in a well-characterized cancer model.

The host HeLa cell line is an immortalized human cervical adenocarcinoma positive for HPV18, widely employed for cancer research. Its epithelial origin and transformation by viral oncoproteins E6 and E7 disrupt p53 and Rb pathways, providing a deregulated proliferative context for studying pathways involved in tumorigenesis, metastasis, and drug response.

DPP9 is a serine protease that removes N-terminal dipeptides from substrates with Pro or Ala at the penultimate position, influencing immune regulation, apoptosis, and cell adhesion. DPP9 is activated by IFN-?? and TNF-?? and functions downstream of NF-??B. It processes neuropeptide Y (NPY) and glucagon-like peptide-1 (GLP-1), and its activity modulates CXCL10 expression, linking protease function to inflammatory signaling. DPP9 interacts with DPP8 and forms dimers. Loss of DPP9 leads to substrate accumulation, altered peptide hormone degradation, and impacts on immune and apoptotic pathways.

In HeLa cells, DPP9 knockout impacts tumor-relevant phenotypes. DPP9 modulates cell adhesion and migration, contributing to metastatic potential. Its role in antigen presentation may affect immune recognition, while altered apoptosis signaling could influence chemosensitivity. This model enables exploration of DPP9’s functions in cervical cancer progression and its interplay with HPV-mediated oncogenesis.

These polyclonal cells are suited for cancer biology, immune regulation, protease function analysis, and drug target validation. Representative assays include DPP enzymatic activity with Gly-Pro-AMC, western blot, RT-qPCR, apoptosis and migration assays, flow cytometry, and CXCL10 ELISA. Cell viability screens and cytokine profiling further support mechanistic and therapeutic studies. For additional inquiries or to place an order, please contact Ascent Research.

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