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Cat. No. ARG34153

ITFG2 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

CRISPR/Cas9-edited ITFG2 Knouckout A-549 Polyclonal Cells provide a heterogeneous loss-of-function model in a human lung adenocarcinoma cell line. ITFG2 is an integrin-associated protein that links T-cell receptor?CCD28 co-stimulation, NF-??B, and integrin/FAK signaling pathways, and its disruption perturbs adhesion, migration, and survival cascades including PI3K/Akt and MAPK. Applications include integrin signaling studies, metastasis drug screening, and tumor microenvironment research, using techniques such as western blotting, adhesion assays, and phospho-signaling analysis of FAK, Akt, and ERK. This product is ideal for cancer biologists and immunology researchers exploring integrin-mediated pathology.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A549

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    Lung

    Gene Name

    ITFG2

    Gene Identifier

    NCBI Gene ID 55846

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    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 ITFG2 Knouckout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of ITFG2 in the A-549 human lung adenocarcinoma cell line. This heterogeneous pool of edited cells enables robust gene-function analyses without clonal-selection artifacts, making it ideal for cancer biology and signal transduction research.

A-549 is a widely used model for non-small cell lung carcinoma, established from a 58-year-old Caucasian male. Its epithelial nature and retention of key oncogenic pathways, including integrin signaling, make it an appropriate host for investigating adhesion, migration, and tumor progression.

ITFG2 encodes an integrin-associated protein known to function downstream of T-cell receptor stimulation and CD28 co-stimulation in lymphoid cells, regulated by NFAT and NF-??B. It interacts with integrin alpha chains and focal adhesion kinase (FAK), positioning it at a nexus between adhesive and growth-factor signaling. In A-549, ITFG2 disruption likely impairs integrin activation and dampens PI3K/Akt and MAPK cascades, altering NF-??B and AP-1 transcriptional responses. Canonical mediators include the TCR?CZAP-70?CLAT?CSLP-76 axis, ITK, PLC??1, PKC??, CARMA1?CBCL10?CMALT1, IKK, JNK, and AP-1, many of which also participate in adhesion and survival pathways in epithelial cells.

This A-549 ITFG2 knockout population offers a physiologically relevant system for dissecting mechanisms of lung adenocarcinoma cell adhesion, migration, and invasion. Loss of ITFG2 may uncover vulnerabilities in integrin-dependent survival signals that drive metastatic dissemination, facilitating the identification of novel therapeutic targets. The polyclonal format preserves genetic heterogeneity, enabling robust, statistically powered screens and dose-response studies.

Applications include western blotting, RT-qPCR, and Sanger sequencing for knockout validation; immunofluorescence for focal adhesion proteins; adhesion, migration, and invasion assays; and phospho-signaling analysis of pFAK, pAkt, and pERK. Flow cytometry can quantify surface integrin expression, while apoptosis and viability assays evaluate cell fate. Transcriptomic profiling via RNA-seq can reveal global pathway rewiring. These cells are well suited for integrin signaling research, drug target screening for anti-metastatic compounds, and tumor microenvironment investigations. For further details, please contact Ascent Research.

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