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Cat. No. ARG40482

EDIL3 Knockout K562 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Pleural effusion

  • Disease:

    Chronic myeloid leukemia

EDIL3 Knockout K-562 Polyclonal Cells are CRISPR/Cas9-edited polyclonal knockout cells derived from the human CML line K-562, with disrupted EDIL3 gene function. EDIL3, a secreted matricellular protein, binds integrins ??v??3/??v??5 to activate FAK/PTK2 and downstream PI3K/AKT and MAPK pathways, promoting adhesion and angiogenesis, and is regulated by HIF1A, TNF, and VEGF. Ideal for studying EDIL3-mediated integrin signaling, tumor angiogenesis, and paracrine effects via Western blotting, phospho-FAK analysis, and tube formation assays, this model supports drug discovery and functional genomics investigations in cancer and vascular biology.

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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

    EDIL3

    Gene Identifier

    NCBI Gene ID 10085

    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

EDIL3 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human chronic myeloid leukemia suspension line K-562. The product features disruption of the EDIL3 gene via CRISPR/Cas9-mediated gene editing, yielding a heterogeneous pool of cells with loss-of-function mutations. This polyclonal format enables functional studies without clonal isolation, providing a practical model for population-level analyses.

K-562 cells, established from a 53-year-old female with CML in blast crisis, harbor the BCR-ABL fusion oncogene and exhibit multipotent hematopoietic progenitor properties. Widely used to investigate leukemia biology and signal transduction, this suspension line offers a relevant background for examining EDIL3 function in hematopoietic malignancies and integrin-mediated adhesion pathways.

EDIL3 encodes a secreted matricellular protein that binds integrin receptors ??v??3 and ??v??5, activating focal adhesion kinase (FAK/PTK2) and downstream SRC?CPI3K?CAKT and HRAS?CRAF1?CMAP2K1?CMAPK3 cascades to promote cell adhesion, migration, and angiogenesis. EDIL3 transcription is induced by HIF1A, TNF, IL1B, TGFB, and VEGF. The protein interacts with extracellular matrix components such as fibronectin and vitronectin, and its engagement of integrins triggers phosphorylation of key signaling nodes including AKT1 and ERK.

In the K-562 background, EDIL3 knockout disrupts autocrine/paracrine integrin signaling, enabling dissection of EDIL3-dependent adhesion dynamics independent of endothelial-specific outputs. The multipotent hematopoietic character allows exploration of EDIL3??s role in progenitor adhesion and the leukemic microenvironment, while conditioned media from these cells can be used to test paracrine effects on stromal or vascular cells.

Researchers can apply EDIL3 Knockout K-562 Polyclonal Cells for functional studies of EDIL3 in tumor angiogenesis via tube formation assays with conditioned media, or for investigation of integrin signaling through phospho-FAK/AKT analysis and cell adhesion assays. The model is suited for drug screening, RNA-seq profiling, and analysis of EDIL3 secretion by ELISA. For additional information, contact Ascent Research.

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