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Phenotypes Associated with This Genotype
Genotype
MGI:3039512
tg2
Allelic
Composition
Tg(Alb1-Ren)2Unc/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Alb1-Ren)2Unc mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 60% of transgenic males die suddenly between 6 and 8 months of age

behavior/neurological
• transgenic mice drink significantly more than non-transgenic mice

cardiovascular system
• transgenic mice have: increased left ventricle/body weight ratios; increased cardiac myocyte cross-sectional area; generalized fibrosis; decreased left ventricular end systolic dimension coupled with increased cardiac function, indicating that these mice have concentric hypertrophy, without ventricular dilation or overt heart failure
• in mice that die prematurely a prolonged and progressive bradycardia is seen
• transgenics show a significant decrease in heart rate variability compared to wild-type mice
• transgenic mice have blood pressures more than 25 mmHg higher than wild-type mice (J:88650)
• transgenic mice have blood pressures more than 25 mmHg higher than wild-type mice (J:89252)
• administration of an angiotensin II receptor antagonist lowered blood pressure in transgenic mice down to that seen in wild-type mice (J:89252)

homeostasis/metabolism
• serum creatinine is elevated in transgenic mice
• transgenic mice produce dilute urine but are able to produce concentrated urine following water deprivation
• urine protein/creatinine ratios are elevated and an increase in albumin in the urine of transgenic mice is seen
• administration of an angiotensin II receptor antagonist improved this condition

immune system
• vascular, glomerular, and tubointerstitial changes indicative of hypertensive nephrosclerosis are seen in transgenic mice
• cortical sections show inflammatory infiltrates, fibroid necrosis and arterial disruption
• administration of an angiotensin II receptor antagonist ameliorated these pathological changes

renal/urinary system
• transgenic mice produce dilute urine but are able to produce concentrated urine following water deprivation
• urine protein/creatinine ratios are elevated and an increase in albumin in the urine of transgenic mice is seen
• administration of an angiotensin II receptor antagonist improved this condition
• vascular, glomerular, and tubointerstitial changes indicative of hypertensive nephrosclerosis are seen in transgenic mice
• cortical sections show inflammatory infiltrates, fibroid necrosis and arterial disruption
• administration of an angiotensin II receptor antagonist ameliorated these pathological changes

growth/size/body
• transgenic mice have: increased left ventricle/body weight ratios; increased cardiac myocyte cross-sectional area; generalized fibrosis; decreased left ventricular end systolic dimension coupled with increased cardiac function, indicating that these mice have concentric hypertrophy, without ventricular dilation or overt heart failure


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
12/10/2024
MGI 6.24
The Jackson Laboratory