Fbp2 Conditional Knockout mouse models

The muscle-predominant fructose-1,6-bisphosphatase is encoded by Fbp2, ortholog of human FBP2, which hydrolyzes fructose-1,6-bisphosphate during glyconeogenesis, allowing lactate carbon to be resynthesized into glycogen after intense contraction. The Fbp2 protein is markedly more AMP sensitive than the liver isoform and additionally associates with aldolase, mitochondria and nuclei, where it has been reported to stabilize mitochondrial membrane potential and restrain apoptosis, activities separable from gluconeogenic catalysis. The allele fork therefore matters: a conditional null in skeletal muscle or cardiomyocytes tests glycogen resynthesis and recovery kinetics, whereas point mutants that break either the AMP site or the aldolase interaction dissociate catalysis from the reported protective role. Because Fbp1 covers liver and kidney, whole-body glucose homeostasis will often look normal, so avoid systemic glycemia as a primary readout. Instead match allele to muscle glycogen repletion, mitochondrial respirometry and postexercise recovery, using tamoxifen-inducible Cre to bypass developmental adaptation.

Conditional deletion of Fbp2 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 Fbp2 floxed stock yields usable cohorts.