The IKBKE Knockout HeLa Polyclonal Cells product comprises a heterogeneous population of HeLa cells harboring CRISPR/Cas9-mediated disruption of the IKBKE gene. This polyclonal knockout model provides a loss-of-function tool for studying IKBKE-dependent signaling pathways without the limitations of clonal selection.
HeLa cells are an immortalized human cervical adenocarcinoma cell line positive for human papillomavirus type 18 (HPV18), established from a cervical carcinoma. They serve as a robust and extensively characterized model for cancer biology, virology, and signal transduction research, offering a relevant cellular context for investigating IKBKE functions in inflammation and oncogenesis.
IKBKE encodes IKK??, a non-canonical I??B kinase that functions downstream of viral RNA sensors RIG-I and MDA5 and adaptor MAVS. Upon activation by upstream kinases such as TBK1 and scaffold proteins TRAF3 and TANK, IKBKE directly phosphorylates transcription factors IRF3 and IRF7, inducing their dimerization and nuclear translocation to drive type I interferon production. Additionally, IKBKE contributes to NF-??B activation via TLR3/TRIF-dependent pathways, linking innate immune sensing to inflammatory and oncogenic gene expression programs.
In HeLa cells, which retain functional innate immune signaling machinery, disruption of IKBKE impairs the phosphorylation of IRF3/IRF7 and attenuates type I interferon induction following viral infection or TLR3 stimulation. This model allows dissection of IKBKE-dependent and -independent branches of antiviral immunity and reveals the kinase??s role in modulating NF-??B-driven transcription, thereby affecting cell proliferation, apoptosis, and proinflammatory cytokine profiles. It is particularly valuable for studying cross-talk between innate immunity and oncogenic pathways in an HPV-positive cervical cancer background.
These polyclonal IKBKE knockout HeLa cells are suitable for diverse experimental approaches, including Western blot analysis of IKBKE and downstream targets such as phospho-IRF3 and I??B??, RT-qPCR quantification of interferon-stimulated genes like IFN-?? and ISG15, and IFN-?? luciferase reporter assays. They enable functional studies of IKBKE in antiviral responses using infection models with VSV or Sendai virus, as well as cell proliferation (MTT) and apoptosis (Annexin V) assays to explore oncogenic roles. Additionally, the model supports co-immunoprecipitation studies of IKBKE interactors like TBK1 and IRF3, and high-throughput inhibitor screening. For further product details or technical consultation, please contact Ascent Research.