The IFIT1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the IFIT1 gene in A-549 human lung adenocarcinoma cells. Created through CRISPR/Cas9-mediated gene disruption, this polyclonal model provides a loss-of-function system for studying interferon-induced antiviral responses. The heterogenous population avoids clonal bias and is suitable for high-throughput and functional genomic applications.
The A-549 cell line originates from a 58-year-old male lung adenocarcinoma patient and displays adherent epithelial morphology. It is a standard model for lung cancer biology and respiratory viral infection studies, including influenza and SARS-CoV-2. These cells retain key alveolar epithelial characteristics, making them relevant for investigating innate immune signaling in pulmonary disease.
IFIT1 is an interferon-stimulated gene encoding a sensor of viral RNA. It binds 5′-triphosphate or cap-0 RNA lacking 2′-O-methylation, inhibiting viral translation and replication. Expression is induced by type I/III IFNs via JAK-STAT activation of ISGF3 (STAT1-STAT2-IRF9) and IRF3/7. Upstream, RIG-I and MDA5 recognize viral RNA, signaling through MAVS to activate TBK1/IKK??, which phosphorylate IRFs. IFIT1 interacts with IFIT2 and IFIT3 to form antiviral complexes, and it targets eIF3 and STING to block translation and amplify IFN responses.
In A-549 cells, IFIT1 knockout provides a platform to dissect interferon-dependent antiviral mechanisms in lung epithelium. It is particularly suited for studying host-pathogen interactions with respiratory viruses and exploring the roles of IFIT proteins in interferon amplification and STING cross-talk. This model also supports research into tumor-intrinsic innate immunity and oncolytic virus therapies.
Applications include viral infectivity assays, interferon stimulation experiments, RT-qPCR, western blotting, and RNA-seq to define IFIT1-dependent transcriptional networks. Co-immunoprecipitation identifies IFIT1 interaction partners in its absence. The cells facilitate antiviral drug screening targeting the RIG-I/MDA5?CMAVS pathway and cancer immunology studies on interferon-induced tumor modulation. For further details, please contact Ascent Research.
