The ATF2 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the A-549 lung adenocarcinoma cell line, featuring targeted disruption of the ATF2 gene. This polyclonal knockout model is generated using CRISPR/Cas9-mediated gene editing to introduce loss-of-function mutations across the ATF2 locus, resulting in a heterogeneous population of cells with disrupted ATF2 expression. The product provides a flexible and efficient system for studying ATF2-dependent biology without the clonal selection artifacts associated with single-cell-derived lines.
The host A-549 cell line originates from a 58-year-old Caucasian male with lung adenocarcinoma and serves as a well-established in vitro model of alveolar Type II pneumocytes. A-549 cells retain key characteristics of lung epithelial cancer, including active MAPK and NF-??B signaling, and are widely used in respiratory disease research, drug discovery, and cancer cell biology studies. This cellular background offers a physiologically relevant platform for investigating transcription factor function in lung adenocarcinoma pathogenesis and stress signaling.
ATF2 is a basic leucine zipper (bZIP) transcription factor that functions as a central node in cellular stress responses. It is activated by upstream kinases JNK and p38 following stimulation by growth factors such as EGF, cytokines like TNF-??, or environmental stresses including UV radiation and oxidative stress. Phosphorylated ATF2 forms heterodimers with c-Jun, JunB, JunD, or CREB and recruits coactivators such as p300/CBP to regulate target gene expression. ATF2 transcriptionally controls diverse effectors including cyclin D1 for cell cycle progression, PD-L1 for immune evasion, matrix metalloproteinases for invasion, and Bcl-2 family members for apoptosis regulation, while interacting with NF-??B and Smad3 to integrate multiple signaling cascades.
In A-549 lung adenocarcinoma cells, ATF2 participates in oncogenic signaling networks that drive proliferation, survival, and metastatic potential. Knockout of ATF2 disrupts these transcriptional programs, providing a loss-of-function model to dissect ATF2??s role in lung cancer progression. The polyclonal nature of the knockout population enables the study of ATF2-dependent effects in a genetically diverse cell pool, reflecting more physiological heterogeneity. Researchers can use this model to investigate how ATF2 ablation alters stress-induced apoptosis, cytokine production, migration, and responses to chemotherapeutic agents in a lung cancer context.
This polyclonal knockout cell product is suited for a range of experimental applications including transcriptional profiling via RNA-seq, protein expression analysis by western blotting and immunofluorescence, functional assays such as apoptosis and cell cycle flow cytometry, migration and invasion studies, and chromatin immunoprecipitation to map ATF2 target occupancy. The cells can also be employed in drug sensitivity screens and luciferase reporter assays for AP-1/CRE activity. By enabling robust characterization of ATF2-dependent pathways, the model supports lung cancer research, stress signaling dissection, and drug target validation. For further technical specifications or ordering information, please contact Ascent Research.
