Rela Conditional Knockout mouse models

Rela encodes p65, the ortholog of human RELA and the principal transactivating subunit of canonical NF-kappaB, which dimerizes with p50 through its Rel homology domain, is retained in the cytoplasm by IkappaB alpha, and enters the nucleus after IKK beta phosphorylates IkappaB alpha and triggers its ubiquitin-dependent degradation, with Ser536 and Ser276 phosphorylation and p300 acetylation tuning output at kappaB elements. Germline deletion is embryonic lethal at midgestation from TNF-driven hepatocyte apoptosis, a lethality rescued by concurrent Tnfrsf1a deficiency, which is a useful genetic maneuver but shifts the inflammatory baseline. Conditional nulls with hepatocyte, myeloid or intestinal epithelial Cre drivers are therefore standard for inflammation and tumor promotion endpoints, while phospho-site or transactivation domain knockins separate nuclear entry from cofactor recruitment. Rel and Relb do not substitute for p65 in canonical target induction, so compensation is limited and single-locus phenotypes are usually interpretable.

Rela conditional knockout mice carry a floxed allele so you delete function only where Cre is active. The germline allele stays intact until you cross to a tissue specific Cre. Labs reach for this design when a global knockout is lethal, when they need adult onset loss, or when regional redundancy hides a whole body phenotype.