The ANXA11 Knockout A-549 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population in which the ANXA11 gene has been disrupted. This genetically heterogeneous pool of A-549 cells provides a powerful loss-of-function model for investigating ANXA11-dependent processes. The polyclonal format retains the natural diversity of CRISPR/Cas9-mediated editing events, allowing researchers to study the collective impact of ANXA11 disruption without clonal selection bias. It is suited for experiments where population-level phenotypes are relevant, such as signaling studies, drug response profiling, or autophagy assays.
The host cell line A-549 is a well-characterized human epithelial cell line derived from a lung carcinoma of a 58-year-old Caucasian male. These cells are widely used as a model for human alveolar type II epithelial cells and lung adenocarcinoma biology. They exhibit typical epithelial morphology and retain key signaling pathways, making them a robust platform for cancer research and for studying lung epithelial cell functions, including surfactant production and response to cellular stress.
ANXA11 encodes a calcium-dependent phospholipid-binding protein that functions as a critical regulator of cell cycle progression, apoptosis, and vesicle trafficking. It is activated by calcium influx and cellular stress signals, and it operates within mTOR signaling, autophagy, and calcium signaling pathways. Mechanistically, ANXA11 interacts with PDCD6 (ALG-2), S100A6 (calcyclin), and RACK1, and it modulates downstream targets such as cyclin D1 and caspases. Through these interactions, ANXA11 promotes cell cycle progression while also contributing to apoptosis regulation. In the context of neurodegenerative disease, ANXA11 has been implicated in the aggregation of TDP-43, a hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.
In A-549 lung adenocarcinoma cells, ANXA11 disruption offers a relevant model to dissect its dual roles in cancer cell survival and stress responses. These cells are frequently employed to investigate apoptosis evasion mechanisms, autophagy regulation, and cell cycle defects. The knockout of ANXA11 in this background enables the examination of its contribution to lung adenocarcinoma biology, including proliferation and resistance to therapy. Moreover, because ANXA11 links to TDP-43 pathology, these cells provide a unique system to investigate the intersection of cancer cell biology and neurodegeneration-related aggregation processes.
This polyclonal knockout cell population is ideal for a range of research applications, including the study of ALS disease mechanisms, the regulation of apoptosis and autophagy, and cancer cell biology. Representative assays include western blotting for ANXA11 and TDP-43 to confirm knockout and assess aggregation, immunofluorescence for protein localization, Annexin V apoptosis assays, autophagy flux measurements, RT-qPCR for gene expression changes, and flow cytometry for cell cycle analysis. In drug discovery, these cells can be used to screen compounds targeting ANXA11-related pathways for ALS and lung cancer. For further technical information, please contact Ascent Research.
