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Cat. No. ARG41131

ELAVL2 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The ELAVL2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HeLa cervical adenocarcinoma line, engineered for targeted disruption of the ELAVL2 gene. This loss-of-function model enables investigation of the neuronal RNA-binding protein ELAVL2, which stabilizes ARE-containing mRNAs encoding factors such as FOS and JUN, in a cancer cell context. The polyclonal knockout format preserves population heterogeneity and is ideal for studying post-transcriptional gene regulation, mRNA stability, and ELAVL2??s role in cancer and neurodegenerative disease. Key applications include luciferase reporter assays, RNA immunoprecipitation, and transcriptomic profiling.

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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

    ELAVL2

    Gene Identifier

    NCBI Gene ID 1993

    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 ELAVL2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ELAVL2 gene. This heterogeneous pool of HeLa cells contains diverse loss-of-function mutations, offering a model for studying ELAVL2-dependent processes without clonal selection biases. The polyclonal format is advantageous for investigating post-transcriptional regulation in a context that maintains population-level genetic diversity.

The HeLa host line, an immortalized cervical adenocarcinoma cell line established in 1951, is widely used for gene-editing studies. Its genome harbors HPV18 sequences that inactivate p53 and Rb via E6 and E7 oncoproteins, providing a cellular environment with compromised tumor suppressor pathways. This background is particularly relevant for research on cancer biology and stress responses.

ELAVL2 is an RNA-binding protein that recognizes AU-rich elements (AREs) in 3?? UTRs, stabilizing and enhancing translation of bound mRNAs. It governs the expression of neuronal and stress-responsive genes, including FOS, JUN, GAP43, BCL2, and BDNF. Its activity is regulated by upstream signals like neurotrophin signaling and transcription factors NEUROD1 and ASCL1, and it collaborates with ELAVL1, ELAVL3, ELAVL4, PABPC1, and AGO2 in multiprotein regulatory complexes.

In HeLa cells, ELAVL2 knockout decouples its RNA-regulatory functions from neuronal context, enabling dissection of ARE-mediated mechanisms in a carcinoma background. This is salient because ELAV proteins are frequently aberrantly expressed in cancers, and HeLa??s p53/Rb deficiency may intersect with ELAVL2-regulated pathways controlling cell survival and proliferation. The model thus provides insights into post-transcriptional contributions to malignancy.

Researchers can use these cells for luciferase reporter assays tracking ARE-dependent mRNA stability, RIP to identify ELAVL2 targets, and RT-qPCR, RNA-seq, or western blot to profile molecular changes. Flow cytometry facilitates population-level phenotypic analyses. The knockout is applicable to drug discovery efforts aimed at modulating mRNA turnover. For additional details, contact Ascent Research.

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