Rara Conditional Knockout mouse models

Rara is the mouse ortholog of human RARA and encodes retinoic acid receptor alpha, a nuclear receptor with AF-1, zinc finger DNA-binding, and ligand-binding domains that heterodimerizes with RXR on direct-repeat retinoic acid response elements, holds targets repressed through NCoR, SMRT, and HDAC complexes when unliganded, and switches to p300 and NCOA coactivators upon all-trans retinoic acid binding. The dominant disease logic is fusion driven, since PML-RARA in acute promyelocytic leukemia converts the receptor into a constitutive repressor that blocks myeloid maturation and is resolved pharmacologically by retinoid-induced degradation. Accordingly, allele choice diverges sharply between conditional nulls for tissue retinoid requirements, dominant-negative or PML-RARA knockins for leukemia modeling, and humanized ligand-binding domains for agonist and degrader pharmacology. Rarb and Rarg compensate extensively, and only compound receptor alleles reproduce full vitamin A deficiency phenotypes, so plan multi-locus conditional genetics with an inducible driver from the outset.

Conditional deletion of Rara 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 Rara floxed stock yields usable cohorts.