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Cat. No. ARG42540

CASP8AP2 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The CASP8AP2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-engineered polyclonal population with disrupted CASP8AP2 (FLASH) in HeLa human cervical cancer epithelial cells. CASP8AP2 is a crucial scaffold for extrinsic apoptosis, histone pre-mRNA processing, and NF-??B signaling, interacting with caspase-8 and CDK2. This knockout model facilitates research on death receptor-mediated apoptosis, histone mRNA metabolism, and antiviral innate immunity using assays such as western blotting, apoptosis detection, reporter gene analysis, and RNA-seq. It is a valuable tool for cancer biology and signal transduction studies.

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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

    CASP8AP2

    Gene Identifier

    NCBI Gene ID 9994

    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 CASP8AP2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from HeLa human cervical adenocarcinoma epithelial cells. This loss-of-function model provides a heterogeneous pool of CASP8AP2-deficient cells, enabling robust functional analyses of the FLASH scaffold protein. By disrupting CASP8AP2, this product facilitates the study of apoptosis regulation, histone mRNA processing, NF-??B signaling, and antiviral innate immunity without residual wild-type protein interference.

HeLa cells are an immortalized epithelial line originally isolated from a cervical adenocarcinoma and characterized by integrated HPV-18 genome sequences. Their transformed phenotype, sustained proliferation, and well-documented genetic background make them a standard model in cancer biology, signal transduction research, and virology. The polyclonal CASP8AP2 knockout population preserves these intrinsic properties while eliminating functional CASP8AP2 expression, allowing direct comparative studies with parental HeLa cells.

CASP8AP2 (FLASH) is a scaffold protein that facilitates caspase-8 activation via FADD downstream of death receptors, leading to caspase-3/7 cleavage in extrinsic apoptosis. It is also essential for histone pre-mRNA 3??-end processing, binding U7 snRNP and CPSF components. Additionally, CASP8AP2 modulates NF-??B signaling and antiviral responses, with its functions regulated by CDK2 and interferon pathways.

Within the HeLa cellular context, CASP8AP2 ablation provides a valuable model to investigate the intersection of apoptosis, cell cycle control, and histone metabolism. The presence of HPV-18 oncoproteins that inactivate p53 and Rb renders these cells particularly dependent on coordinated histone synthesis, making CASP8AP2 knockout a valuable tool for studying replication-coupled gene expression. Furthermore, loss of FLASH may sensitize these cancer cells to death receptor ligands, offering insights into mechanisms of drug resistance and apoptotic evasion.

This polyclonal knockout population is suited for apoptosis detection via Annexin V and TUNEL, caspase cleavage western blotting, NF-??B luciferase reporter assays, and histone mRNA processing analysis by RT-qPCR or RNA-seq. Flow cytometry for cell cycle profiling and antiviral innate immunity studies further broaden its utility. It is an adaptable platform for cancer biology, immunology, and drug development. Please contact Ascent Research for further information.

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