Analysis Tools
immune system
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• mice show decreased susceptibility to intranasal infection with severe acute respiratory syndrome coronavirus (SARS-CoV; Beijing strain, PUMC01 isolate)
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Allele Symbol Allele Name Allele ID |
Ace2tm1Pngr targeted mutation 1, Josef M Penninger MGI:2661723 |
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| Summary |
11 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice show decreased susceptibility to intranasal infection with severe acute respiratory syndrome coronavirus (SARS-CoV; Beijing strain, PUMC01 isolate)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exposed to caecal ligation and perforation (CLP) to cause sepsis-induced acute lung injury show decreased survival compared to controls, with only 2 of 10 mice surviving the 6 hour experimental period compared to 100% survival in wild-type mice
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• mice exhibit decreased survival following P. aeruginosa infection
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• mice infected with P. aeruginosa show a greater decrease in body weight than wild-type mice
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• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased lung edema compared to controls
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• acid-treated mice show a greater increase in angiotensin II levels in the lungs than similarly treated controls
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• acid-treated mice show a greater increase in angiotensin II levels in plasma than similarly treated controls
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• mice exposed to caecal ligation and perforation (CLP) to cause sepsis-induced acute lung injury show decreased survival compared to controls, with only 2 of 10 mice surviving the 6 hour experimental period compared to 100% survival in wild-type mice
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• mice exhibit enhanced acute lung injury after acid aspiration, cecal ligation and perforation (CLP), or endotoxin challenge compared to controls
• mice exposed to acid aspiration show worsened oxygenation, massive lung edema, increased inflammatory cell infiltration and hyaline membrane formation compared to controls
• CLP-treated mutant mice show worsening of lung function, increased edema, and leukocyte accumulation
• pharmacological inhibition of angiotensin II type 1 receptor with Losartan attenuates the severity of acid-induced lung injury
• however, inhibition of angiotensin II type 2 receptor with PD123.319 has no effect on the acute lung injury
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• mice infected with P. aeruginosa exhibit increased neutrophil infiltration in the lungs
• mice infected with P. aeruginosa and treated with an IL-17A-neutralizing antibody show more neutrophil infiltration to the lungs
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• mice infected with P. aeruginosa exhibit increased neutrophil infiltration in the lungs
• mice infected with P. aeruginosa and treated with an IL-17A-neutralizing antibody show more neutrophil infiltration to the lungs
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• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased inflammatory cell infiltration and leukocyte accumulation, respectively, compared to controls
(J:100334)
• mice infected with P. aeruginosa show increased lung inflammation, showing an accumulation of neutrophils
(J:282139)
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• mice infected with P. aeruginosa exhibit weight loss, enhanced lung permeability, increased neutrophil infiltration into the lungs, reduced bacterial outgrowth in bronchoalveolar lavage fluid, and exaggerated lung inflammation and lung injury compared to controls
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• mice exhibit decreased survival following P. aeruginosa infection
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• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased lung edema compared to controls
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• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased inflammatory cell infiltration and leukocyte accumulation, respectively, compared to controls
(J:100334)
• mice infected with P. aeruginosa show increased lung inflammation, showing an accumulation of neutrophils
(J:282139)
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• mice exposed to acid aspiration show hyaline membrane formation
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• mice exposed to acid aspiration, CLP or endotoxin challenge to induce acute lung injury show greater lung elastance compared to controls
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• mice exposed to acid aspiration show greatly increased pulmonary vascular permeability
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• less severe than in age matched mutant male mice
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• less severe than in age matched mutant male mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice infected with live H5N1 avian flu virus die more quickly than infected wild-type controls
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• H5N1 virus-infected mice show increased inflammatory cell infiltration compared to controls
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• mice show increased susceptibility to H5N1 avian flu virus (A/chicken/Jilin/9/2004) infection, showing higher viral load in lungs 5 days after infection and greater lung injury, including increased alveolar wall thickness, formation of hyaline membranes, and proteinaceous debris filling the airspaces
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• mice infected with live H5N1 avian flu virus die more quickly than infected wild-type controls
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• H5N1 virus-infected mice show greater lung edema at 3 days post infection than wild-type controls
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• H5N1 virus-infected mice show greater lung edema at 3 days post infection than wild-type controls
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• H5N1 virus-infected mice show increased inflammatory cell infiltration compared to controls
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• H5N1 virus-infected mice show formation of hyaline membranes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• similar to Acetm1Unc homozygotes however normal cardiac contractility is seen at 6 months of age unlike in Acetm1Unc homozygotes
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• mice exposed to acid aspiration to induce acute lung injury show decreased angiotensin II levels in lung compared to single Ace2tm1Pngr mutants
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• mice exposed to acid aspiration to induce acute lung injury show decreased angiotensin II levels in plasma compared to single Ace2tm1Pngr mutants
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• mice show rescue of severe lung failure, edema formation, and histological lung changes induced by acid aspiration in single Ace2tm1Pngr mutants
• mice show rescue of the severe lung impairments seen in single Ace2tm1Pngr mutants with endotoxin-induced acute lung injury
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• similar to Acetm1Unc homozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• similar to Acetm1Unc homozygotes however normal cardiac contractility is seen unlike Acetm1Unc homozygotes
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• mice exposed to acid aspiration to induce acute lung injury show decreased angiotensin II levels in lung compared to single Ace2tm1Pngr mutants
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• mice exposed to acid aspiration to induce acute lung injury show decreased angiotensin II levels in plasma compared to single Ace2tm1Pngr mutants
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• mice show rescue of severe lung failure, edema formation, and histological lung changes induced by acid aspiration in single Ace2tm1Pngr mutants
• mice show rescue of the severe lung impairments seen in single Ace2tm1Pngr mutants with endotoxin-induced acute lung injury
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• similar to Acetm1Unc homozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increase in basal myocardial contractility
• mice exhibit a partial reversal of myocardial hypertrophy, prevention of neutrophil infiltration into myocardial tissue, and prevention of systolic function deterioration
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• increase in basal myocardial contractility
• mice exhibit a partial reversal of myocardial hypertrophy, prevention of neutrophil infiltration into myocardial tissue, and prevention of systolic function deterioration
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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N |
• heart angiotensin II levels are not elevated and superoxide production is normal indicating lack of oxidative stress in aged mice
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• mice show decreased susceptibility to intranasal infection with severe acute respiratory syndrome coronavirus (SARS-CoV; Beijing strain, PUMC01 isolate)
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
• mice exposed to caecal ligation and perforation (CLP) to cause sepsis-induced acute lung injury show decreased survival compared to controls, with only 2 of 10 mice surviving the 6 hour experimental period compared to 100% survival in wild-type mice
|
|
|
• mice exhibit decreased survival following P. aeruginosa infection
|
|
|
• mice infected with P. aeruginosa show a greater decrease in body weight than wild-type mice
|
|
|
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased lung edema compared to controls
|
|
|
• acid-treated mice show a greater increase in angiotensin II levels in the lungs than similarly treated controls
|
|
|
• acid-treated mice show a greater increase in angiotensin II levels in plasma than similarly treated controls
|
|
|
• mice exposed to caecal ligation and perforation (CLP) to cause sepsis-induced acute lung injury show decreased survival compared to controls, with only 2 of 10 mice surviving the 6 hour experimental period compared to 100% survival in wild-type mice
|
|
|
• CLP-treated mutant mice show worsening of lung function, increased edema, and leukocyte accumulation
• mice exposed to acid aspiration show worsened oxygenation, massive lung edema, increased inflammatory cell infiltration and hyaline membrane formation compared to controls
• mice exhibit enhanced acute lung injury after acid aspiration, cecal ligation and perforation (CLP), or endotoxin challenge compared to controls
• pharmacological inhibition of angiotensin II type 1 receptor with Losartan attenuates the severity of acid-induced lung injury
• however, inhibition of angiotensin II type 2 receptor with PD123.319 has no effect on the acute lung injury
|
|
|
• mice infected with P. aeruginosa exhibit increased neutrophil infiltration in the lungs
• mice infected with P. aeruginosa and treated with an IL-17A-neutralizing antibody show more neutrophil infiltration to the lungs
|
|
|
• mice infected with P. aeruginosa exhibit increased neutrophil infiltration in the lungs
• mice infected with P. aeruginosa and treated with an IL-17A-neutralizing antibody show more neutrophil infiltration to the lungs
|
|
|
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased inflammatory cell infiltration and leukocyte accumulation compared to controls
(J:100334)
• mice infected with P. aeruginosa show increased lung inflammation, showing an accumulation of neutrophils
(J:282139)
|
|
|
• mice infected with P. aeruginosa exhibit weight loss, enhanced lung permeability, increased neutrophil infiltration into the lungs, reduced bacterial outgrowth in bronchoalveolar lavage fluid, and exaggerated lung inflammation and lung injury compared to controls
|
|
|
• mice exhibit decreased survival following P. aeruginosa infection
|
|
|
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased lung edema compared to controls
|
|
|
• mice exposed to acid aspiration, CLP, or endotoxin challenge show increased inflammatory cell infiltration and leukocyte accumulation compared to controls
(J:100334)
• mice infected with P. aeruginosa show increased lung inflammation, showing an accumulation of neutrophils
(J:282139)
|
|
|
• mice exposed to acid aspiration show hyaline membrane formation
|
|
|
• mice exposed to acid aspiration, CLP, or endotoxin challenge to induce acute lung injury show greater lung elastance compared to controls
|
|
|
• mice exposed to acid aspiration show greatly increased pulmonary vascular permeability
|
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• development of cardiomyopathy is associated with eccentric hypertrophy as indicated by increased left ventricle weight normalized to tibial length or body weight
• hearts show upregulation of hypertrophic disease markers ANF and BNP
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• slight thinning of the left ventricular wall resulting in mild dilation, 6 months of age
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• ventricular dilation at 6 and 12 months of age
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• progressive left ventricular dilation and reduced systolic function with increasing age
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• age-dependent and progressive decline in cardiac function
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• development of cardiomyopathy is associated with eccentric hypertrophy as indicated by increased left ventricle weight normalized to tibial length or body weight
• young mice treated with the specific AT1 receptor blocker, irbesartan, until 12 months of age prevents the development of dilated cardiomyopathy at 6 months and persists until 12 months of age
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• more severe at 6 months of age than at 3 months of age
(J:77232)
• more severe in 6 month old males than in age matched female mutant mice
(J:77232)
• decrease in fractional shortening and velocity of circumferential shortening corrected for heart rate, decreased peak aortic velocity corrected for heart rate
(J:124548)
• rightward displacement of the pressure-volume curve indicating reduced systolic function
(J:124548)
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• echocardiography indicates increased left ventricular end diastolic and systolic dimension, decreased fractional shortening, decreased velocity of circumferential shortening corrected for heart rate, decreased peak aortic velocity corrected for heart rate, increased left ventricle end diastolic pressure, and decreased maximum and minimum first derivative of the left ventricle pressure (+dP/dt and dP/dt)
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• increase in left ventricle end diastolic pressure
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• reduced blood pressure observed at 6 months of age
• blood pressure was normal at 3 months of age
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• 4-fold increase in neutrophil infiltration in the myocardium of aged mice
• however, no macrophage infiltration into the myocardium is seen
• treatment with irbesartan prevents neutrophil infiltration in the myocardium
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• development of cardiomyopathy is associated with eccentric hypertrophy as indicated by increased left ventricle weight normalized to tibial length or body weight
• hearts show upregulation of hypertrophic disease markers ANF and BNP
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• myocardial aldehyde levels are increased in mice indicating chronic myocardial oxidative damage
• treatment with irbesartan normalizes myocardial aldehyde levels
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• increase in expression of inflammatory cytokines, IL-1beta, IL-6, and MCP-1 in aged mice
• treatment with irbesartan prevents increased expression of inflammatory cytokines
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• NADPH oxidase activity is increase in the left ventricle of 6 month old mice
• mice treated with irbesartan to block AT1 suppresses the increase in NADPH oxidase activity
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• development of cardiomyopathy is associated with eccentric hypertrophy as indicated by increased left ventricle weight normalized to tibial length or body weight
• young mice treated with the specific AT1 receptor blocker, irbesartan, until 12 months of age prevents the development of dilated cardiomyopathy at 6 months and persists until 12 months of age
|
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• more severe at 6 months of age than at 3 months of age
(J:77232)
• more severe in 6 month old males than in age matched female mutant mice
(J:77232)
• decrease in fractional shortening and velocity of circumferential shortening corrected for heart rate, decreased peak aortic velocity corrected for heart rate
(J:124548)
• rightward displacement of the pressure-volume curve indicating reduced systolic function
(J:124548)
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• 4-fold increase in neutrophil infiltration in the myocardium of aged mice
• however, no macrophage infiltration into the myocardium is seen
• treatment with irbesartan prevents neutrophil infiltration in the myocardium
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• increase in expression of inflammatory cytokines, IL-1beta, IL-6, and MCP-1 in aged mice
• treatment with irbesartan prevents increased expression of inflammatory cytokines
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| congestive heart failure | DOID:6000 | J:124548 | ||
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
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• mice infected with live H5N1 avian flu virus die more quickly than infected wild-type controls
|
|
|
• H5N1 virus-infected mice show increased inflammatory cell infiltration compared to controls
|
|
|
• mice show increased susceptibility to H5N1 avian flu virus (A/chicken/Jilin/9/2004) infection, showing higher viral load in lungs 5 days after infection and greater lung injury, including increased alveolar wall thickness, formation of hyaline membranes, and proteinaceous debris filling the airspaces
|
|
|
• mice infected with live H5N1 avian flu virus die more quickly than infected wild-type controls
|
|
|
• H5N1 virus-infected mice show greater lung edema at 3 days post infection than wild-type controls
|
|
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• H5N1 virus-infected mice show greater lung edema at 3 days post infection than wild-type controls
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• H5N1 virus-infected mice show increased inflammatory cell infiltration compared to controls
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• H5N1 virus-infected mice show formation of hyaline membranes
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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 04/16/2024 MGI 6.23 |
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