S100a9 Conditional Knockout mouse models

Encoding MRP14 (calgranulin B), S100a9 is the mouse ortholog of human S100A9 and pairs with S100A8 through a hydrophobic interface to build the calprotectin heterodimer, then assembles into calcium-dependent tetramers that are the receptor-active species for TLR4 and RAGE. The protein carries a C-terminal extension with an additional metal site and a phosphorylation-regulated segment, and it directs the complex to membranes and to the NADPH oxidase during neutrophil activation, while extracellular tetramers drive chemotaxis, beta 2 integrin affinity maturation, and metal sequestration that restricts microbial growth. Nulls are viable but lose S100A8 protein as well, which confounds subunit-specific conclusions and argues for tetramerization-deficient or metal-site knockins alongside myeloid conditional alleles. Because mice lack S100a12, calgranulin biology cannot be fully reconstructed without human transgenes. Match the allele to endpoints such as sepsis mortality, autoimmune arthritis, or tumor myeloid suppression.

Conditional deletion of S100a9 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 S100a9 floxed stock yields usable cohorts.