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Cat. No. ARG42519

CASP7 Knockout huh-7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Hepatocellular carcinoma

The CASP7 Knockout Huh-7 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population in Huh-7 human hepatocellular carcinoma cells, establishing a heterogeneous loss-of-function model. Huh-7, a widely used liver cancer cell line, supports hepatitis C virus replication and recapitulates hepatocyte biology. Disruption of CASP7, an executioner caspase activated by initiator caspases (CASP8, CASP9) and granzyme B, removes a critical effector of apoptosis regulated by XIAP. This product is well-suited for apoptosis signaling studies, liver cancer drug screening, and hepatocyte death pathway analysis, using techniques such as DEVD-ase activity assays, western blotting for cleaved caspase-7, and flow cytometry with Annexin V/7-AAD.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Huh-7

    Sex of Donor

    Male

    Age

    57 years

    Gene Name

    CASP7

    Gene Identifier

    NCBI Gene ID 840

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    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 CASP7 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in Huh-7 human hepatocellular carcinoma cells, providing a heterogeneous pool of CASP7-disrupted cells. This loss-of-function model avoids clonal selection, enabling robust functional studies of caspase-7-dependent apoptosis signaling.

Huh-7 is a well-differentiated hepatocellular carcinoma cell line derived from a 57-year-old Japanese male. It retains hepatocyte features and is widely used as a model for liver cancer biology and hepatitis C virus (HCV) replication, making it valuable for studying hepatic oncogenesis and viral-host interactions.

CASP7 encodes the executioner caspase-7, which is proteolytically activated by initiator caspases such as CASP8, CASP9, and CASP10, as well as granzyme B. Activation occurs downstream of death receptor ligands (e.g., TRAIL, FasL) or mitochondrial cytochrome c release and APAF1 apoptosome assembly. Once active, caspase-7 cleaves key substrates including PARP1, DFFA, lamin A/C, gelsolin, and BID, thereby dismantling cellular structures and promoting cell death. Its activity is tightly controlled by inhibitor of apoptosis proteins, particularly XIAP, while SMAC/DIABLO relieves this inhibition. This places CASP7 at a critical nexus of intrinsic and extrinsic apoptotic pathways.

In Huh-7 hepatocellular carcinoma, CASP7 knockout enables systematic dissection of apoptosis resistance mechanisms commonly observed in liver cancer. The model facilitates evaluation of how loss of this executioner caspase influences cell survival, drug sensitivity, and viral cytopathicity, given Huh-7’s permissiveness to HCV. It also aids investigation of hepatocyte death in liver fibrosis and inflammatory conditions, where caspase-7 signaling is increasingly recognized.

These polyclonal knockout cells are ideally suited for apoptosis signaling studies, liver cancer drug screening, and HCV-host interaction research in a hepatic context. Researchers can assess caspase-7 activity using fluorogenic DEVD-ase assays, confirm cleavage via western blotting, and measure apoptosis by flow cytometry with Annexin V and 7-AAD. Additional applications include TUNEL staining for DNA fragmentation, MTT cell viability assays, and immunofluorescence detection of active caspase-7. For further technical information, please contact Ascent Research.

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