Mapk1 Conditional Knockout mouse models

Mapk1, the mouse ortholog of human MAPK1, encodes ERK2, the more abundant of the two classical extracellular signal-regulated kinases, activated by MEK1 and MEK2 phosphorylation of the Thr and Tyr residues in its TEY motif and directing substrate choice through a common docking groove and an F-site that recognize DEF and D-domain motifs in Rsk kinases, Elk1, Fos, and Myc, where it phosphorylates Ser62 to stabilize the protein; Dusp6 and Spry proteins impose negative feedback. Homozygous nulls die in early gestation from trophoblast and placental failure, so conditional alleles are required, and allele class separates questions cleanly: floxed deletion tests tissue dependence, an analog-sensitive gatekeeper mutant enables acute kinase inhibition without adaptive rewiring, and knock-in reporters such as kinase translocation constructs quantify signaling dynamics rather than presence. Mapk3-encoded ERK1 is a genuine paralog whose null is viable, and total ERK dosage rather than isoform identity governs most phenotypes, so plan compound alleles accordingly.

Conditional deletion of Mapk1 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 Mapk1 floxed stock yields usable cohorts.