Pkm Conditional Knockout mouse models

Pkm, the mouse ortholog of human PKM, encodes pyruvate kinase M and is regulated principally by mutually exclusive splicing of exon 9 versus exon 10, controlled by PTBP1 and by hnRNPA1 and hnRNPA2, yielding either the constitutively active PKM1 tetramer typical of differentiated tissue or PKM2, whose tetramer to dimer equilibrium responds to fructose 1,6-bisphosphate, serine, phosphotyrosine peptides and acetylation. The low-activity PKM2 dimer throttles the terminal glycolytic step, backing upstream intermediates into biosynthetic branches and underpinning the Warburg phenotype, with additional nuclear functions reported. Consequently, isoform-selective engineering matters more than deletion: exon-specific alleles that force PKM1 or PKM2 expression test the splicing hypothesis directly, while conditional nulls address whether the locus is required at all in a given lineage. The Pklr paralog covers liver and erythroid tissue only. Match the allele to lactate flux, biosynthetic tracing or tumor initiation endpoints with tissue-matched Cre drivers.

Conditional deletion of Pkm 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 Pkm floxed stock yields usable cohorts.