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. ARG0494

ZNF750 Knockout KYSE-150 Cell Line

  • Product Type:

    Genome-edited Cells

  • Tissue Source:

    Esophagus

  • Disease:

    Squamous cell carcinoma

  • Gene Species:

    Homo sapiens (Human)

The ZNF750 Knockout KYSE-150 Cell Line is a CRISPR/Cas9-edited knockout cell line targeting ZNF750, a transcription factor and tumor suppressor that drives terminal epidermal differentiation downstream of TP63. ZNF750 activates cornified envelope genes (IVL, LOR, FLG) and the lipid barrier gene ABCA12, cooperating with KLF4 and CEBPA. This model utilizes the poorly differentiated KYSE-150 ESCC line to enable functional studies of ZNF750 in squamous cell carcinogenesis. Applications include expression profiling, ChIP, and phenotypic assays for migration, invasion, and drug sensitivity. Contact Ascent Research for more 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

    KYSE-150

    Morphology

    Epithelial-like

    Age

    49 years

    Sex of Donor

    Female

    Gene Name

    ZNF750

    Gene Species

    Homo sapiens (Human)

    Gene Identifier

    NCBI Gene ID 79755

  • 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 ZNF750 Knockout KYSE-150 Cell Line is a CRISPR/Cas9-edited knockout cell line that provides a stable loss-of-function model for investigating the transcriptional tumor suppressor ZNF750 in esophageal squamous cell carcinoma (ESCC). Generated by CRISPR/Cas9-mediated gene disruption of ZNF750 in the KYSE-150 parental line, this homogeneous knockout cell line enables reproducible functional studies and is suitable for a wide range of molecular and cellular assays. KYSE-150 is a poorly differentiated human esophageal squamous cell carcinoma line originally derived from a 49-year-old male patient. These cells retain hallmark features of malignant esophageal squamous epithelial cells, including loss of terminal differentiation and aggressive growth properties, making them a physiologically relevant model for studying factors that regulate ESCC pathogenesis and differentiation. ZNF750 functions as a master transcription factor downstream of TP63 and NOTCH signaling, driving terminal epidermal differentiation. It directly activates genes encoding structural components of the cornified envelope, such as involucrin (IVL), loricrin (LOR), and filaggrin (FLG), as well as the lipid transporter ABCA12, which is critical for barrier formation. ZNF750 cooperates with KLF4 and CEBPA and interacts with the co-repressor RCOR1. Disruption of this network by ZNF750 knockout impairs barrier integrity and promotes squamous carcinogenesis. This knockout model is particularly valuable for dissecting the TP63?CZNF750?CKLF4 regulatory axis in ESCC. By comparing knockout and parental cells, researchers can assess ZNF750-dependent changes in gene expression, cell cycle progression, migration, and invasion. The model also allows investigation of how ZNF750 loss alters responses to upstream regulators such as NOTCH1 and AP-1, and how it influences the expression of late differentiation markers and sensitivity to chemotherapeutic agents. Standard applications include Western blotting and RT?qPCR for ZNF750 and its targets (IVL, LOR, FLG), RNA?seq for transcriptome profiling, ChIP?qPCR for mapping ZNF750 occupancy at genomic targets, immunofluorescence for cornified envelope proteins, and functional assays such as cell migration, invasion, and drug sensitivity testing by MTT and colony formation. This knockout cell line serves as an essential tool for advancing ESCC research and screening for differentiation?inducing therapeutics. For additional details or ordering, 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)