These Abca1^fl/fl Abcg1^fl/fl double floxed mice possess loxP sites flanking exons 45-46 of the ATP-binding cassette, sub-family A (ABC1), member 1 (Abca1) gene and loxP sites flanking exon 3 of the ATP-binding cassette, sub-family G (WHITE), member 1 (Abcg1) gene. Two loxP-flanked neomycin resistance cassettes are still present in these mice, and the donating investigator reports that they do not effect protein expression in macrophages. ABCA1 controls the assembly of phospholipids and free cholesterol with lipid-free Apolipoprotein A-I (apoA-I) to form high density lipoprotein (HDL) and also mediates cholesterol efflux to apolipoproteins and small, pre-beta HDL particles from peripheral cells. Mutations in Abca1 are associated with Tangier disease and familial hypoalphalipoproteinemia, which are characterized by near absence of plasma HDL and the accumulation of cholesterol esters in tissues. ABCG1 is involved in cholesterol and phospholipid efflux to large, mature HDL particles, and regulates cellular lipid homeostasis. Mice that are homozygous for these alleles are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have Abca1 exons 45-46 and Abcg1 exon 3 deleted in cre-expressing tissues.

For example, when crossed to B6.129P2-Lyz2^tm1(cre)Ifo/J mice (Stock No. 004781) expressing Cre recombinase in the myeloid cell lineage, including monocytes, mature macrophages, and granulocytes, resulting mice display an increase in hematopoietic stem and multipotential progenitor cell (HSPC) mobilization and extramedullary hematopoiesis.

When crossed to C57BL/6J-Tg(Itgax-cre,-EGFP)4097Ach/J mice (Stock No. 007567) expressing Cre recombinase in dendritic cells, resulting mice display an increase in blood colony forming units, IL17 and IL23 secretion.