The ID3 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population derived from A-549 human lung adenocarcinoma cells, with targeted disruption of the ID3 gene. This product delivers a heterogeneous pool of cells bearing diverse gene-editing outcomes, enabling robust functional studies of ID3 loss-of-function without the artifacts of single-cell cloning. The polyclonal nature reduces clonal selection bias and provides a representative sampling of knockout effects across the population.
A-549 cells, established from a human lung adenocarcinoma, are a standard model of alveolar basal epithelial cells. They retain key traits of type II pneumocytes, including surfactant production, and are extensively used in lung cancer biology, respiratory toxicology, and antiviral research. Their inherent epithelial-mesenchymal plasticity makes them particularly suitable for studying EMT-related processes and tumor metastasis.
ID3 is a dominant-negative inhibitor of basic helix-loop-helix (bHLH) transcription factors including E47 (TCF3), E2-2 (TCF4), and HEB (TCF12). By forming transcriptionally inactive heterodimers, it prevents these factors from binding E-box sequences and activating targets such as p21. ID3 expression is induced by TGF-beta/SMAD2/3, BMP/SMAD1/5/8, Notch, and c-Myc, and it integrates proliferative signals through interactions with RB1 and Ets-1, suppressing differentiation and senescence.
Disrupting ID3 in the A-549 adenocarcinoma background provides a direct means to examine its contribution to lung cancer pathogenesis. Loss of ID3 is expected to de-repress E-proteins, leading to p21 upregulation and reinstatement of cell cycle arrest and senescence programs. This model therefore allows dissection of ID3??s role in sustaining proliferation and evading senescence, offering insights into therapeutic strategies targeting ID3 or its downstream effectors.
The polyclonal knockout cells are well-suited for a range of experimental techniques, including proliferation and migration assays, senescence detection via SA-beta-gal staining, and protein or transcript profiling by western blotting, RT-qPCR, and RNA-seq. Flow cytometry and immunofluorescence enable phenotypic characterization. They support investigations in lung adenocarcinoma, stem cell and vascular biology, immunology, and senescence research. For additional information, contact Ascent Research.
