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Cat. No. ARG41126

ELAVL1 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

ELAVL1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from human cervical carcinoma HeLa cells, engineered for disruption of the ELAVL1 gene encoding the HuR RNA-binding protein. HuR stabilizes ARE-containing mRNAs of critical regulators such as CCND1 and VEGFA, downstream of stress-activated kinases like p38 MAPK. This knockout model facilitates investigation of post-transcriptional gene regulation in cancer biology, including HuR??s roles in proliferation, apoptosis, and stress response. Suited for assays such as RIP, luciferase reporters, and phenotypic readouts, it serves as a valuable tool for RNA biology and drug discovery research.

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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

    ELAVL1

    Gene Identifier

    NCBI Gene ID 1994

    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 ELAVL1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the HeLa cell line, providing a loss-of-function model for the ELAVL1 gene encoding the RNA-binding protein HuR. The polyclonal format ensures a heterogeneous knockout pool, enabling robust functional analysis without clonal bias. This product is optimized for studies in post-transcriptional gene regulation, cancer biology, and cellular stress responses.

HeLa cells are an immortalized, HPV18-positive cervical adenocarcinoma epithelial cell line with aneuploid karyotype, widely used for genetic manipulation and phenotypic screening due to their well-characterized biology, rapid growth, and extensive literature support. Disrupting ELAVL1 in this background allows investigation of HuR function in a cancer-relevant context where mRNA stability control is frequently dysregulated.

ELAVL1 encodes HuR, which binds AU-rich elements (AREs) in 3?? UTRs of target mRNAs, protecting them from degradation and enhancing translation. HuR is activated by upstream kinases including p38 MAPK, PKC, and AMPK in response to cellular stressors like hypoxia and cytokines. It stabilizes key transcripts such as CCND1, VEGFA, MYC, BCL2, PTGS2, and TP53, and interacts with regulators like AUF1, TTP, and CRM1 to modulate mRNA fate. This post-transcriptional network rapidly adjusts expression of proliferation, survival, and inflammatory genes.

In HeLa cells, where HuR is often overexpressed, its knockout enables dissection of its contributions to malignant phenotypes, including uncontrolled proliferation and apoptosis resistance. This model is highly valuable for exploring how HuR-dependent mRNA stabilization drives cervical carcinoma progression and for identifying therapeutic vulnerabilities.

This polyclonal knockout product supports a wide range of experimental approaches, including RT-qPCR and RNA immunoprecipitation to assess target mRNA levels and HuR binding, actinomycin D chase and dual-luciferase reporter assays for mRNA stability and ARE activity, western blotting and immunofluorescence for protein expression and localization, and cell viability, proliferation, and apoptosis assays (e.g., annexin V staining). These cells are ideally suited for studies in RNA biology, cancer signaling, and drug target discovery. For further information, please contact Ascent Research.

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