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Cat. No. ARG37453

HNRNPR Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The HNRNPR Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HeLa cervical adenocarcinoma line (HPV18-positive). This model disrupts HNRNPR, an RNA-binding protein that interacts with the SMN complex and regulates SMN and ??-actin mRNAs, providing a powerful tool for post-transcriptional regulation research. Knockout-mediated disruption of mRNA processing and transport enables functional studies in neurodegenerative diseases, cervical cancer, and RNA metabolism. Typical applications include RNA immunoprecipitation, RT-qPCR, western blotting, and cell proliferation assays to interrogate HNRNPR-dependent phenotypes.

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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

    HNRNPR

    Gene Identifier

    NCBI Gene ID 10236

    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 HNRNPR Knockout HeLa Polyclonal Cells product provides a CRISPR/Cas9-mediated knockout population of HeLa cells, delivering a versatile loss-of-function model for studying HNRNPR. This polyclonal pool, rather than a clonal isolate, maintains genetic heterogeneity and is generated through targeted disruption of the HNRNPR gene, impairing protein expression. The model is optimized for reproducible research outcomes in RNA biology, cancer research, and neurodegenerative disease studies.

The HeLa cell line is a human cervical adenocarcinoma line with epithelial morphology and is HPV18-positive. Isolated from a cervical tumor, HeLa cells are a classic model in cancer biology, virology, and cellular biochemistry. Their rapid growth, transfectability, and extensive characterization make them ideal for generating knockout models to probe gene function in a cancerous epithelial context. The HPV18 background provides additional relevance for exploring interactions between viral oncoproteins and host RNA processing machinery.

HNRNPR encodes an RNA-binding protein that regulates mRNA processing, transport, and stability. It assembles into ribonucleoprotein complexes with the SMN protein, Gemin proteins, and other hnRNPs. Key target transcripts include SMN mRNA and ??-actin mRNA. HNRNPR acts downstream of general transcription factors and cellular stress cues. Its disruption compromises SMN complex formation and alters the expression and localization of target mRNAs, perturbing RNA metabolic networks.

In HeLa cells, HNRNPR knockout illuminates how RNA-binding protein dysfunction intersects with cancer biology. Loss of HNRNPR may dysregulate post-transcriptional control of mRNAs involved in proliferation, stress, and apoptosis, which are relevant to cervical adenocarcinoma pathology. Additionally, HNRNPR’s links to amyotrophic lateral sclerosis and spinal muscular atrophy position this model at the interface of cancer and neurodegeneration research, enabling comparative studies of RNA processing pathways shared between these diseases.

Applications include RT-qPCR and RNA immunoprecipitation to assess mRNA processing, western blotting for protein analysis, immunofluorescence for localization, and functional assays for proliferation and apoptosis. This polyclonal knockout model is ideal for comparing RNA metabolism alterations versus wild-type HeLa cells, aiding in the dissection of HNRNPR-dependent mechanisms in stress granule dynamics and splicing. For technical inquiries and custom experimental design, please contact Ascent Research.

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