Phenotypes associated with this allele

• Allele Symbol: Nr3c1^tm1.1Jaci
• Allele Name: targeted mutation 1.1, John Cidlowski
• Allele ID: MGI:5526027
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Nr3c1^tm1.1Jaci/Nr3c1^tm1.1Jaci Tg(Myh6-cre)2182Mds/0	involves: C57BL/6 * FVB/N	MGI:5526029

Genotype
MGI:5526029

cn1

• Allelic Composition: Nr3c1^tm1.1Jaci/Nr3c1^tm1.1Jaci; Tg(Myh6-cre)2182Mds/0
• Genetic Background: involves: C57BL/6 * FVB/N

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

mortality/aging

premature death ( J:201995 )

• increase morbidity and mortality by 5 months

• 7 months median survival age

• male mice have a median survival age of 8 months while this is only 6 months for female mice

respiratory system

abnormal lung morphology ( J:201995 )

♂ • free erythrocytes in alveoli and hemosiderin-laden macrophages (heart failure cells) within alveolar spaces (at 6 months of age

respiratory distress ( J:201995 )

growth/size/body

enlarged heart ( J:201995 )

♂ • in nearly all mice examined

increased heart weight ( J:201995 )

♂ • at 3 months of age

cardiac hypertrophy ( J:201995 )

♂

abnormal thoracic cavity morphology ( J:201995 )

♂ • in the majority of mice examined

immune system

heart inflammation ( J:201995 )

♂ • indicated by expression analysis

homeostasis/metabolism

abnormal atrial thrombosis ( J:201995 )

♂ • characterized by lamellation of fibrin and inflammatory cells, chronic inflammation, fibrosis, and neovascularization

abnormal calcium ion homeostasis ( J:201995 )

♂ • isolated cardiomyocytes fail to show a sustained increase in intracellular calcium following exposure to low concentrations of caffeine

muscle

increased myocardial fiber size ( J:201995 )

♂ • about a 140% increase in cardiomyocyte cross-sectional area at 3 months of age

♂ • adrenalectomy at 2 months of age does not reduce the increase in cardiomyocyte size seen at 6 months of age

decreased cardiac muscle contractility ( J:201995 )

♂ • variable decrease in ejection fraction and increase in the left ventricular end-systolic dimension at 3 months of age

cardiovascular system

cardiovascular system phenotype ( J:201995 )

♂N • despite cardiac remodeling and reduced heart function, no electrocardiogram abnormalities are detected in mice at 3 - 6 months of age

increased myocardial fiber size ( J:201995 )

♂ • about a 140% increase in cardiomyocyte cross-sectional area at 3 months of age

♂ • adrenalectomy at 2 months of age does not reduce the increase in cardiomyocyte size seen at 6 months of age

enlarged heart ( J:201995 )

♂ • in nearly all mice examined

increased heart weight ( J:201995 )

♂ • at 3 months of age

cardiac hypertrophy ( J:201995 )

♂

increased heart left ventricle weight ( J:201995 )

♂ • at 3 months of age

dilated heart left ventricle ( J:201995 )

♂ • marked

thick ventricular wall ( J:201995 )

♂ • at 3 months

cardiac fibrosis ( J:201995 )

♂ • associated with atrial thrombosis

♂ • NORMAL: not detected in the ventricular wall at 3 months of age

poor circulation ( J:201995 )

♂ • atrial thrombosis is consistent with atrial blood stasis

decreased cardiac muscle contractility ( J:201995 )

♂ • variable decrease in ejection fraction and increase in the left ventricular end-systolic dimension at 3 months of age

abnormal heart echocardiography feature ( J:201995 )

♂ • no abnormality in 1 month-old mice but byat 3 months, but not at 1 month, mutant mice displays spontaneous LV left ventricular systolic dysfunction.

abnormal myocardial fiber physiology ( J:201995 )

♂ • isolated cardiomyocytes fail to show a sustained increase in intracellular calcium following exposure to low concentrations of caffeine

pathological neovascularization ( J:201995 )

♂ • associated with atrial thrombosis

congestive heart failure ( J:201995 )

♂

heart inflammation ( J:201995 )

♂ • indicated by expression analysis