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Cat. No. ARG36087

HAVCR1 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The HAVCR1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population that disrupts HAVCR1 in the HeLa cervical adenocarcinoma cell line. This model abrogates TIM-1 function, a phosphatidylserine receptor and hepatitis A virus entry factor that signals through PI3K/AKT and NF-??B pathways, regulated by IL-4/STAT6 and affecting AKT, NF-??B, MAPK, and BCL2. Key applications include viral entry studies, apoptosis assays, and investigation of immune signaling cascades. Functional readouts such as phosphatidylserine binding, Annexin V/PI staining, and downstream target expression analysis are facilitated, supporting research in virology, cancer biology, and kidney injury.

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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

    HAVCR1

    Gene Identifier

    NCBI Gene ID 26762

    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 HAVCR1 Knockout HeLa Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the HAVCR1 gene in the HeLa cervical adenocarcinoma cell line. This polyclonal model provides a versatile loss-of-function system for interrogating TIM-1 (HAVCR1) biological functions, reflecting heterogeneous editing outcomes typical of polyclonal populations without single-cell cloning.

HeLa cells, derived from a cervical adenocarcinoma of Henrietta Lacks, are an immortalized human cell line widely employed in cancer biology, virology, and signal transduction research. Their robust proliferation and extensive characterization make them a standard host for gene perturbation studies.

The HAVCR1 gene encodes TIM-1, a phosphatidylserine receptor that mediates phagocytosis of apoptotic cells and serves as a cellular entry receptor for hepatitis A virus and other enveloped viruses. Ligand engagement triggers intracellular signaling through PI3K/AKT and NF-??B pathways. Upstream regulators include IL-4, STAT6, NF-??B, and TGF-??, while downstream targets encompass AKT, NF-??B, MAPK, and BCL2. TIM-1 functionally interacts with phosphatidylserine, forms homodimers, and associates with ITGB1, LCK, and ZAP70. Representative pathway components include HAVCR1??PI3K??AKT, HAVCR1??NF-??B, and HAVCR1??BCL2 family, collectively modulating cell survival, proliferation, and immune responses.

In the HeLa context, HAVCR1 knockout impairs viral entry and apoptotic cell clearance, and potentially alters signaling networks that intersect with T-cell co-stimulatory pathways. This model is particularly valuable for dissecting viral entry mechanisms and apoptosis regulation in a well-characterized human cancer cell background, despite the absence of an endogenous immune repertoire.

Research applications include viral infection assays for hepatitis A and other HAVCR1-dependent viruses, apoptosis analysis using Annexin V/PI staining, phosphatidylserine binding assessed by flow cytometry, and RT-qPCR or Western blotting for downstream targets such as AKT, NF-??B, and BCL2. This knockout product is suitable for studies on immune checkpoint biology, kidney injury, and cancer cell survival. For additional information or custom requests, please contact Ascent Research.

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