Table 1.
Strain name | ACE promoter | Target tissues | BP | Phenotype |
---|---|---|---|---|
ACE 1/1 (ACE null) [15] | Normal ACE promoter but gene inactivated by intragenic neo cassette | No tissues express ACE | Very low | Renal medullary expansion. Inability to concentrate urine. Male infertility. Anemia |
ACE 3/3 [16] | Albumin promoter | Hepatocytes. Normal circulating ACE. 14% normal renal ACE | Normal | None |
ACE 8/8 [17] | α-Myosin heavy chain promoter | Cardiac myocytes. Low circulating ACE. No renal ACE | Low (nearly normal) | Early death due to cardiac arrhythmias. Normal renal phenotype |
ACE 9/9 [18] | Kidney specific cadherin promoter | Renal tubular epithelium | Low | Renal phenotype was similar but milder than ACE null mouse |
ACE 10/10 [19] | c-fms promoter | Myelomonocytic cells. Normal circulating ACE. No renal ACE | Normal | Normal renal phenotype. Enhanced immune response |
ACE, angiotensin-converting enzyme; BP, blood pressure. These mice were created by targeted homologous recombination in embryonic stem cells. ACE expression is determined by the ability of individual tissues to use the promoter positioned to control tissue and temporal activity of the ACE gene.