Ikbke Conditional Knockout mouse models

Ikbke encodes IKK epsilon, the mouse ortholog of human IKBKE and the noncanonical IKK family kinase most closely related to TBK1, sharing a kinase domain, ubiquitin-like domain, and scaffold dimerization region. Together with TBK1 it phosphorylates IRF3 on the C-terminal serine cluster to license interferon beta transcription, and it also phosphorylates STAT1 at Ser708 to reshape ISGF3 output and modifies NF-kB regulators including CYLD, which underlies its behavior as an amplified breast cancer oncogene able to substitute for AKT driven survival signaling. Design follows the question directly: a conditional null removes protein and scaffolding together, whereas a kinase-dead knockin distinguishes catalytic activity from complex assembly, the decisive comparison for evaluating small molecule inhibitors. Substantial redundancy with Tbk1 means single deletion blunts rather than abolishes interferon induction, and because Tbk1 nulls die in utero from TNF driven hepatocyte apoptosis, compound experiments require conditional Tbk1 alleles planned in advance.

Conditional deletion of Ikbke limits the genetic change to the lineage you choose. That helps in oncology, immunology, and metabolic work where systemic loss would muddy the read. After you confirm Cre specificity, crossing to Ikbke floxed stock yields usable cohorts.