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Cat. No. ARG39678

DPP7 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The DPP7 Knockout HeLa Polyclonal Cells provide a polyclonal CRISPR/Cas9-edited HeLa cell population with disrupted DPP7, a lysosomal serine dipeptidyl peptidase controlled by TFEB and involved in apoptosis. This model uses HPV-18-positive cervical adenocarcinoma cells with inactivated p53/Rb, offering a relevant system for studying lysosomal proteolysis and cell death. By eliminating DPP7 activity, researchers can examine its role in peptide processing that influences caspase and Bcl-2 pathways, employing assays such as Annexin V/PI flow cytometry, cleaved caspase-3 western blot, and LAMP1 immunofluorescence. Key applications include lysosomal biology, apoptosis research, and cancer drug screening.

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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

    DPP7

    Gene Identifier

    NCBI Gene ID 29952

    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 DPP7 Knockout HeLa Polyclonal Cells represent a population of HeLa cells engineered via CRISPR/Cas9 to disrupt the DPP7 gene, creating a polyclonal loss-of-function model. This product is intended for research into lysosomal dipeptidyl peptidase activity and its role in apoptosis. By maintaining editing diversity, it supports pooled screening and functional assays without the need for monoclonal selection, offering a practical tool for cancer and cell biology laboratories.

The parental HeLa cell line is a well-characterized human cervical adenocarcinoma epithelial model, originally derived from a cervical cancer patient. HeLa cells are HPV-18 positive and exhibit inactivation of p53 and Rb, along with high aneuploidy. These genetic alterations promote vigorous proliferation and apoptosis resistance, making them an informative host for studying cancer biology and the interplay between oncogenic drivers and lysosomal processes.

DPP7 encodes a lysosomal serine dipeptidyl peptidase that preferentially removes N-terminal dipeptides with Pro or Ala, playing a critical role in terminal peptide degradation and protein turnover. Its expression is controlled by TFEB and lysosomal pH, and its activity is inhibited by serine protease inhibitors such as AEBSF. DPP7 functions alongside cathepsins and TPP1, interacting with lysosomal membrane proteins to hydrolyze peptide substrates. The resulting peptide fragments can modulate apoptotic signaling, potentially intersecting with caspase activation and the Bcl-2 regulatory network.

In HeLa cells, which possess defective apoptosis due to HPV-driven p53 and Rb inactivation, DPP7 disruption allows dissection of how lysosomal peptide processing contributes to apoptotic resistance. Loss of DPP7 may alter peptide intermediates that impact mitochondrial or death receptor pathways, providing a model to study lysosome-dependent sensitization of cancer cells to pro-apoptotic cues. This polyclonal knockout population is thus valuable for investigating crosstalk between lysosomal proteolysis and cell fate, and for screening drugs that exploit lysosomal vulnerabilities in tumors.

Researchers can utilize the DPP7 Knockout HeLa Polyclonal Cells in assays including Annexin V/PI flow cytometry for apoptosis quantification, cleaved caspase-3 western blot for effector caspase activation, LAMP1 immunofluorescence for lysosomal visualization, lysosomal protease activity assays for dipeptidyl peptidase function, and RT-qPCR for TFEB target gene expression. These applications facilitate detailed investigations into lysosomal proteolysis, apoptosis signaling, and cancer drug sensitivity, making the product a versatile tool for discovery research. For further details, contact Ascent Research.

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