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Cat. No. ARG34519

ATF1 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The ATF1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited human polyclonal knockout cell population with targeted disruption of the ATF1 transcription factor gene in A-549 lung adenocarcinoma cells. ATF1 mediates gene expression downstream of cAMP/PKA, MAPK/ERK, and calcium signaling, regulating targets such as cyclin D1 and Bcl-2 to promote survival and proliferation. This polyclonal knockout model is designed for investigating ATF1??s oncogenic functions, stress response pathways, and cAMP/CREB-mediated transcription in lung cancer research. Applications include drug screening, gene expression analysis, and functional assays for apoptosis, migration, and signaling dynamics.

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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

    ATF1

    Gene Identifier

    NCBI Gene ID 466

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% COâ‚‚

  • 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. It 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 ATF1 Knockout A-549 Polyclonal Cells constitute a human CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the ATF1 gene in the A-549 lung adenocarcinoma cell line. This polyclonal knockout product offers a genetically heterogeneous loss-of-function model for studying ATF1-dependent signaling and transcription without clonal selection artifacts. The engineered knockout provides a valuable tool for investigating the functional roles of ATF1 in cancer biology and stress-responsive gene regulation.

The A-549 cell line is a human lung adenocarcinoma epithelial model derived from a 58-year-old Caucasian male. Widely used as a model of alveolar type II pulmonary epithelium, it is a cornerstone in lung cancer research, providing a well-characterized platform for investigations into oncogenic signaling and drug responses.

ATF1 is a bZIP transcription factor that binds cAMP response elements (CRE) to regulate gene expression. It is activated by phosphorylation via PKA, ERK, and CaMK in response to cAMP, MAPK, and calcium signals. Phosphorylated ATF1 recruits coactivators CBP/p300 and CRTC family members to stimulate transcription of target genes including cyclin D1, Bcl-2, survivin, c-Fos, Mcl-1, and VEGF. Through these effectors, ATF1 integrates diverse stimuli to promote cell survival and proliferation.

In A-549 cells, ATF1 contributes to oncogenic transcriptional programs. Disruption of ATF1 in this polyclonal knockout population is expected to impair expression of pro-survival and proliferative genes, potentially sensitizing cells to apoptosis and reducing metastatic traits. This model allows evaluation of ATF1 loss in a heterogeneous cell pool, reflecting tumor heterogeneity, and is valuable for dissecting ATF1??s role in lung adenocarcinoma and identifying therapeutic vulnerabilities.

Applications include the study of cAMP/CREB-regulated transcription, drug screening against ATF1-dependent pathways, and functional analysis of proliferation, apoptosis, and invasion. Representative assays include Western blotting, RT-qPCR, RNA-seq, ChIP-qPCR, viability/apoptosis assays, migration/invasion assays, and CRE-luciferase reporters. The knockout cells are also suitable for co-immunoprecipitation of ATF1 complexes. For more information, please contact Ascent Research.

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