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Cat. No. ARG41136

ELAVL4 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The ELAVL4 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the near-haploid human HAP1 cell line. This loss-of-function model targets ELAVL4, a neuronal RNA-binding protein that stabilizes mRNAs such as GAP-43 and Tau via AU-rich element binding, and functions downstream of neurotrophins NGF and BDNF via the TrkA receptor and MAPK/ERK signaling. Knockout of ELAVL4 in HAP1 cells enables dissection of post-transcriptional gene regulation in neuronal differentiation, synaptic plasticity, and survival. Applications include RT-qPCR, western blotting, differentiation assays, and RNA immunoprecipitation to study neurodegenerative and neurodevelopmental disorders.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    ELAVL4

    Gene Identifier

    NCBI Gene ID 1996

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    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 ELAVL4 Knockout HAP1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of HAP1 cells in which the ELAVL4 gene has been disrupted, creating a loss-of-function model for studying neuronal RNA-binding protein function in a tractable genetic background. This knockout product is provided as a mixed polyclonal population, enabling researchers to investigate gene inactivation effects without clonal selection bias.

The HAP1 host cell line is a near-haploid human cell line derived from the male chronic myeloid leukemia cell line KBM-7. Its near-haploid karyotype simplifies gene editing and functional genomics studies by avoiding the confounding effects of heterozygosity, making HAP1 cells particularly useful for haploid genetic screens and targeted knockout analyses. The cell line retains key signaling pathways and is widely employed in molecular biology and cancer research contexts.

ELAVL4 encodes a neuron-specific RNA-binding protein that selectively recognizes AU-rich elements (AREs) in the 3?? untranslated regions of target mRNAs, stabilizing transcripts such as GAP-43, Tau, and neurofilament mRNAs and enhancing their translation. ELAVL4 function is activated downstream of neurotrophins NGF and BDNF via TrkA receptor signaling through MAPK/ERK and PI3K/AKT pathways, and can also be transcriptionally regulated by NEUROD1 and ASCL1. It interacts with factors including RNA polymerase II, hnRNP A1, KSRP, eIF4E, and PABP to coordinate post-transcriptional gene regulation. The mechanistic ensemble promotes neuronal differentiation, neurite outgrowth, synaptic plasticity, and cell survival.

In the HAP1 cell background, disruption of ELAVL4 provides a simplified model to dissect the gene??s molecular contributions to mRNA stabilization and differentiation without the complexities of a full neuronal genetic network. While HAP1 is a leukemia-derived line, it supports retinoic acid-induced differentiation assays that can partially mimic neuronal-like transcriptional programs, allowing functional readouts of ELAVL4-dependent regulation. This polyclonal knockout population is especially suited for high-throughput screens examining neurotoxic insults, neurotrophin signaling, and neurodegenerative disease targets, as it maintains a near-diploid gene dosage for consistent protein-level comparisons.

Typical applications include RT-qPCR and western blotting to quantify changes in downstream targets such as c-Fos, p21, and Bcl-2 mRNAs and proteins, immunofluorescence imaging of neurite outgrowth following differentiation induction, RNA immunoprecipitation (RIP) to validate ELAVL4?CmRNA interactions, and luciferase reporter assays to assess ARE-mediated transcript stability. The model also supports cell viability studies under oxidative or metabolic stress to evaluate ELAVL4??s role in neuronal survival. For more details and technical specifications, please contact Ascent Research.

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