The IFI16 Knockout HeLa Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the IFI16 gene has been disrupted. IFI16 encodes an innate immune DNA sensor that recognizes double-stranded DNA in the cytoplasm and nucleus, thereby activating antiviral and inflammatory responses. This polyclonal product retains the heterogeneous knockout alleles generated by non-homologous end joining, providing a robust loss-of-function model without clonal selection. The cell population is derived from the HeLa cell line and is designed for functional studies of IFI16 in innate immunity, inflammation, and cancer biology.
HeLa cells are an immortalized cervical epithelial adenocarcinoma line positive for human papillomavirus type 18 (HPV18). They exhibit rapid proliferation and a partially defective DNA damage response due to HPV E6 and E7 oncoproteins. This host is a relevant model for investigating interactions between viral oncoproteins and IFI16-mediated interferon and inflammasome responses.
At the molecular level, IFI16 functions as a cytosolic DNA sensor that, upon binding double-stranded DNA, engages the stimulator of interferon genes (STING) to trigger the TBK1?CIRF3 signaling axis, leading to transcriptional induction of type I interferons such as IFN-??. IFI16 also interacts with the adaptor ASC to form the AIM2 inflammasome, promoting caspase-1 activation and subsequent maturation of interleukin-1?? (IL-1??). Additionally, IFI16 exerts tumor-suppressive functions by physically interacting with p53 and BRCA1 to enhance p53-mediated transcription and apoptosis. Upstream, IFI16 expression and activity are regulated by interferons (IFN-?? and IFN-??), foreign DNA, and DNA damage signals. Thus, IFI16 serves as a nexus between the cGAS?CSTING?CTBK1?CIRF3 pathway and the AIM2?CASC?Ccaspase-1 inflammasome.
In the HeLa cervical cancer context, IFI16 loss-of-function studies are particularly informative because HPV oncoproteins disrupt both interferon signaling and apoptosis. By eliminating IFI16, researchers can dissect how HPV18-positive cells modulate innate immune detection of viral or damaged DNA and assess the impact on p53-dependent cell death. This model enables the investigation of whether IFI16 acts as a barrier to HPV-driven carcinogenesis or influences the tumor immune microenvironment. Furthermore, it allows for the study of DNA damage?Cinduced IFI16 signaling in a cell line with compromised p53 and retinoblastoma protein pathways.
These polyclonal knockout cells are suitable for a broad range of experimental applications, including innate immunity studies in response to synthetic DNA ligands or viral infection (e.g., HSV-1, HIV), inflammasome activation assays measuring caspase-1 cleavage or IL-1?? secretion via ELISA, and interferon pathway analysis by RT-qPCR or western blotting for phospho-TBK1. They can also be employed in drug screens targeting STING, TBK1, or the AIM2 inflammasome, and in flow cytometry?Cbased apoptosis assays. For further details, contact Ascent Research.
