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Cat. No. ARG40547

EEF1A2 Knockout K562 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Pleural effusion

  • Disease:

    Chronic myeloid leukemia

CRISPR/Cas9-edited polyclonal K-562 cells with EEF1A2 gene disruption. EEF1A2 encodes eEF1A2, a tissue-specific translation elongation factor that also regulates actin cytoskeleton, apoptosis, and oncogenic signaling via interactions with mTOR, AKT, MYC, STAT3, BAX, and Bcl-2. This model provides a physiologically relevant CML background for studying leukemia biology, oncogene addiction, and apoptosis regulation. Applications include drug target validation, functional genomics, and mechanistic studies using western blotting, flow cytometry, translation assays, and immunofluorescence. The polyclonal format ensures robust gene-disruption representation for reliable loss-of-function analysis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    K562

    Sex of Donor

    Female

    Derived From Site

    In situ; Pleural effusion

    Gene Name

    EEF1A2

    Gene Identifier

    NCBI Gene ID 1917

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 EEF1A2 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from human chronic myelogenous leukemia K-562 cells with targeted disruption of the EEF1A2 gene. This loss-of-function model enables investigation of the tissue-specific translation elongation factor eEF1A2 in leukemia-relevant processes without clonal selection bias.

The K-562 line, established from a 53-year-old female with CML in blast crisis, contains the Philadelphia chromosome and grows as a highly proliferative suspension culture. It serves as a classic model for studying erythroid and myeloid differentiation, oncogenic signal transduction, and drug sensitivity, offering a physiologically relevant hematopoietic context for EEF1A2 knockout studies.

EEF1A2 encodes eEF1A2, which catalyses GTP-dependent aminoacyl-tRNA delivery to the ribosome. This isoform also contributes to actin cytoskeleton organization, apoptosis inhibition, and oncogenic signaling. Upstream regulators include MYC, STAT3, AKT, mTOR, and ER stress sensors; downstream targets encompass ribosomal translation machinery, ??-actin, and apoptotic regulators like BAX and Bcl-2. Interaction partners include actin filaments, ZPR1, aminoacyl-tRNA, GTP, humanin, and HIV-1 Tat. Within signaling networks, EEF1A2 intersects with the PI3K/AKT/mTOR axis, involving mTOR, AKT, PI3K, S6K1, 4E-BP1, BAX, and Bcl-2. EEF1A2 disruption impairs translation elongation and disrupts cytoskeletal and anti-apoptotic functions, sensitizing cells to apoptotic stimuli.

In K-562 cells, EEF1A2 knockout permits dissection of oncogene addiction and apoptosis regulation in CML. Loss of eEF1A2-mediated translation and survival signaling may alter proliferation and differentiation, providing a platform to study cross-talk between protein synthesis control and cytoskeletal dynamics. This model is relevant for validating EEF1A2 as a target in leukemias and other cancers with dysregulated expression.

These polyclonal knockout cells support a variety of experimental approaches, including functional analysis of EEF1A2 in cancer biology, oncogene addiction studies, drug target validation, and mechanistic investigation of apoptosis and translation regulation. Compatible assays include western blotting, RT-qPCR, cell viability (MTT/CCK-8), Annexin V/PI apoptosis detection, colony formation, puromycin incorporation translation assays, co-immunoprecipitation, immunofluorescence for actin cytoskeleton, and transcriptomic profiling by RNA-seq. For expert technical support or custom project inquiries, please contact Ascent Research.

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