Tab3 Conditional Knockout mouse models

Functioning as the paralog that explains many negative results at the Tab2 locus, Tab3 is the mouse ortholog of human TAB3 and encodes an NZF-containing adaptor that likewise binds K63-linked polyubiquitin and the TAK1 kinase domain to support IL-1, TNF, and TLR driven TAK1 activation, with preferences dictated by receptor context and cell type rather than by a wholly distinct mechanism. Its NZF domain reads ubiquitin chains through a different surface than TAB2, and the two proteins occupy TAK1 in mutually exclusive complexes, which is why acute loss of one is buffered. Germline nulls are viable and largely unremarkable, so informative designs are compound conditional alleles with Tab2, or NZF-inactivating knockins that separate ubiquitin recognition from TAK1 binding within an otherwise intact complex. Given genuine redundancy, never treat a single Tab3 knockout as a TAK1 pathway test, and anchor compound genetics to cytokine transcription, hepatocyte survival, or tumor NF-kB endpoints using validated Cre lines.

Conditional deletion of Tab3 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 Tab3 floxed stock yields usable cohorts.