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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: Curr Opin Nephrol Hypertens. 2014 Mar;23(2):106–112. doi: 10.1097/01.mnh.0000441047.13912.56

Table 1.

ACE gene-targeted mice

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.