Irf3 Conditional Knockout mouse models

Irf3 corresponds to human IRF3 and encodes a constitutively expressed interferon regulatory factor with an N-terminal winged helix DNA binding domain and a C-terminal IRF association domain held autoinhibited until TBK1 or IKK epsilon phosphorylate the serine-rich tail at Ser386 and Ser396 downstream of STING, MAVS, or TRIF. Phosphorylation drives dimerization, nuclear accumulation, CBP and p300 recruitment, and transcription of Ifnb1 with early interferon stimulated genes, while a transcription independent arm, the RLR induced apoptotic pathway, uses BH3 like engagement of BAX to kill infected cells. Allele forks map cleanly onto these functions: conditional nulls test requirement, phosphomimetic constitutively active knockins model chronic interferon tone, and mutations separating transactivation from BAX binding isolate the apoptotic arm. Irf7 substantially overlaps in interferon induction, so compound Irf3 with Irf7 deletion is usually required before output is truly abolished, and STING gain-of-function crosses need conditional alleles to survive breeding.

Conditional deletion of Irf3 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 Irf3 floxed stock yields usable cohorts.